HALVERSON & ORS v DOBLER HALVERSON by his tutor v DOBLER

HIS HONOUR : There are four proceedings before the court. The plaintiff, Kurt Halverson, by his tutor (his father, Ken Halverson), sues his general practitioner, Dr Kenneth Dobler, claiming damages for negligence. Kurt alleges that the defendant failed to exercise due care in the treatment of him from 1995 until 10 February 2001. On 11 February 2001 Kurt suffered a cardiac arrest and hypoxic brain damage leaving him with catastrophic injuries. The other proceedings are brought by Kurt’s father, Ken, Kurt’s mother, Janet, and sister, Annika, who each claim damages for nervous shock. (Throughout these reasons I have referred to the submissions made on behalf of Kurt. Those submissions are, of course, also made on behalf of the other plaintiffs).

The essence of the plaintiff’s case was that Dr Dobler should have identified Kurt as having a cardiac problem before he suffered the catastrophic event of 11 February. It was submitted that there were a number of occasions (and I will discuss each of them) when Kurt’s symptoms could have and, it was submitted, should have caused Dr Dobler to refer him to a cardiologist for assessment. It was also submitted that Dr Dobler should have carried out, or ordered to be carried out, an electrocardiogram (ECG) following the various events but most significantly after the detection of a heart murmur followed by a further syncopal event on 4 February 2001. The failure to take either of these steps was identified as a breach of Dr Dobler’s duty of care to Kurt. It was contended that if either of these steps had been taken Kurt’s cardiac irregularity identified as long QT interval (which has since been verified) would probably have been identified and appropriate responses put in place which would have avoided the catastrophe. Alternatively, it was submitted that if an ECG had been performed there was a real chance that a long QT interval would have been found and Kurt should be compensated for having lost that chance.

If liability in the full amount is found the parties have agreed damages for Kurt in the sum of $8,086,000. On the same basis, damages for Ken have been agreed at $550,000, for Janet at $150,000 and for Annika at $11,500.

The plaintiff was born on 25 September 1982. He is now unable to walk or talk. He came to court on the first day of the hearing so that I could gain an understanding of the surgery he required to his arms and legs following his catastrophic injuries and the general extent of his disabilities. Evidence of previous events in his life, his medical history and relevant incidents was given by his father and grandfather.

The plaintiff’s father gave evidence that Kurt was a relatively healthy young man until the time of his injury. There was an incident, when he was thirteen months of age, when, with a high temperature, he started shaking. This was diagnosed as “febrile convulsions.” Kurt suffered from common childhood illnesses such as bronchitis, chicken pox and sometimes had asthma in the winter. He progressed well at school and did well in his School Certificate. He took some time out from school after the School Certificate and embarked upon his Higher School Certificate year in October 2000. During that year he formed a close relationship with his girlfriend Megan McKay.

In his adolescent years Kurt played sport, including basketball, tennis, touch football and cross-country running. Although he had a history of migraine headaches, he was described by his father as having a high level of aerobic fitness prior to his cardiac arrest.

There are a number of events in Kurt’s medical history which are significant in resolving the present claim. It is necessary to both separately describe them and make findings as to their significance having regard to the response made by the defendant to each of them. However before doing so I have included a lexicon of relevant medical terms with a view to making my reasons intelligible to both medical practitioners and lay readers. Lexicon of medical terms Arrhythmia: An abnormal heart rhythm. Auscultation: The process of listening to the heart, usually with a stethoscope. Bradycardia: A slow pulse. This is generally accepted to occur when the pulse rate is below sixty beats per minute. EBV (Epstein-Barr Virus): Causes infectious mononucleosis (glandular fever). ECG (electrocardiogram; Also known as an EKG): The standard ECG is a 12-lead ECG, which involves attaching electrodes to the limbs of a patient, as well as on pre-determined places across the chest wall. This gives a tracing of the electrical conduction system of the patient’s heart. A Holter monitor ECG is used when a patient is to be monitored continuously. This typically involves the use of only one lead. Echocardiogram: An echocardiogram is basically an ultrasound of the heart. It looks at the structure of the heart, the dimensions of the various chambers, the configuration and action of the valves and it assesses flow across valves. It gives an indication of cardiac function by measuring the degree to which the various chambers contract at various stages of the cardiac cycle. An echocardiogram usually involves a contemporaneous single-lead ECG. EEG (electroencephalogram): A neurological investigation that is used, inter alia, to test for epilepsy. Endocarditis: Endocarditis is a condition where there is a bacterial infection on the inside of the heart, typically affecting the valves of the heart. There are two general manifestations. One is the growth of what are called vegetations, or small wart-like projections, usually on the valve, but it may also proceed to the formation of an abscess on the valve. Febrile: Affected by a fever; having a high temperature. Long QT Syndrome (LQTS): Every time a heart beats, an electrical current passes through it. In recording the heart’s electrical conduction, an ECG records a series of peaks and troughs or “waves”. The QT interval is the space between the Q wave and the T wave. Once a current has passed through the heart, it needs to “repolarise.” The QT interval represents the amount of time it takes for ventricular repolarisation to occur. During repolarisation, no current can be conducted. The longer this takes (ie the longer the QT interval), the greater the likelihood that the current will seek an abnormal pathway for conduction, which may cause life-threatening ventricular arrhythmias. The QT interval is measured in milliseconds. A corrected QT measurement (known as the QTc) is used by cardiologists to assess the length of a person’s QT interval. A normal QTc for a male is less than 440 milliseconds and less than 450 milliseconds for a female. A higher QTc is considered to be prolonged. Not all people with LQTS will produce a long QT interval on an ECG all of the time. Professor Saul gave evidence that “in this syndrome we know that 25 to 30 per cent of patients actually have a normal EKG at various times.” The four cardiologists who gave evidence before me concurrently adopted the following definition of LQTS in their joint report: “Long QT syndrome is a complex range of conditions. It is not a single disease with a single outcome. It can be caused by genetic factors, environmental factors or a combination of the two. Environmental factors include drugs, electrolyte abnormalities, myocardial ischaemia, brain injury, bradycardia, hypothermia and stressors which activate the sympathetic nervous system. Regardless of the cause there is a risk of death due to abnormal heart rhythms. The prevalence of the genetic condition is probably in the order of 1 in 3000 of the population. A precise diagnosis of Long QT Syndrome can be difficult to make.” Heart murmur: Normally, the heart makes two regular sounds. The first sound is the closing of the mitral and tricuspid valves, and the second sound is the closure of the aortic and pulmonary valves. A heart murmur is an extra sound that can indicate problems with the heart. Murtagh’s General Practice : A medical text commonly available to and used by Australian general practitioners at the time of Kurt Halverson’s injuries. The 1998 edition was referred to throughout the trial, particularly the chapter titled “Fits, faints and funny turns.” Myocarditis: An inflammatory process of the heart muscle itself. In contrast, endocarditis involves inflammation of the lining membrane of the heart. In rare cases, myocarditis can be secondary to an EBV infection. Prodromal events: These are premonitory signs that typically precede benign syncopal events (i.e. vasovagal events and episodes of postural hypotension). Dr Silberberg, a cardiologist, described them as “the cornerstone of diagnosis” in terms of distinguishing between benign syncopes and syncopes with a cardiological cause. He said: “…sudden cardiac events tend to be like switching a light off…[T]here is no chance – no warning of any type, whereas with vasovagal attacks…[t]here is a considerable period of time, always long enough to have a conversation, to say something – it might just be, ‘I’m not feeling well, I’m going to black out.’ But that is the key. When you get that, you are almost never dealing with a ventricular arrhythmia in that situation, because there has been time for some adjustment.” Syncope: A brief loss of consciousness. Broadly speaking there are three causes of syncope. Dr Dobler stated that “syncope could be broken down into vasovagal events and episodes of postural hypotension, neurological events or cardiac events.” Vasovagal events and episodes of postural hypotension are typically treated as a single category, and were sometimes referred to in evidence as “simple faints.” These syncopes are benign and are usually associated with changes in posture (eg suddenly standing up) or common triggers such as pain, the sight of blood or standing upright for long periods of time. They are usually preceded by premonitory or “prodromal” signs, which enable a person to avoid falling in an awkward or dangerous manner when they lose consciousness. Syncopal events due to neurological or cardiological causes are not benign. Technically, a loss of consciousness with a neurological cause is classified as a seizure rather than as a syncopal event, but for ease of reference they were spoken of in the trial as though they were a type of syncope. An epileptic fit is an example of a loss of consciousness with a neurological cause. Cardiogenic syncope can be caused by a cardiac arrhythmia. Cardiogenic syncope is usually sudden and involves no premonitory signs, or, at most, premonitory signs that are very brief. Consequently it is often accompanied by physical injury suffered when the patient unexpectedly collapses. Professor Saul, a cardiologist, said that recurrent cardiogenic syncope “is the primary symptom of the long QT Syndrome that precedes any sort of malignant events,” but the fact that syncope is recurrent does not of itself indicate that the syncope has a cardiogenic cause. Tachycardia: A fast pulse. LQTS predisposes a person to arrhythmias, particularly ventricular tachycardia. In his report of 24 March 2006, Dr Raftos states that “ventricular tachycardia is a regular contraction of the ventricles at abnormally high rates. The heart does not fill adequately after each contraction and so the cardiac output drops, the supply of blood to the brain drops, and the patient may collapse unconscious, recovering promptly when the cardiac rhythm spontaneously reverts to normal. If the cardiac output is not reduced to the level at which unconsciousness occurs, the patient may present with palpitations, shortness of breath, anxiety, sweating, nausea, or a feeling of general malaise. Episodes of ventricular tachycardia may last from seconds to days. Most episodes of ventricular tachycardia revert spontaneously.” Torsades de pointes: a distinctive type of tachyarrhythmia which can be indicative of LQTS. 4 September 1995 – and medical investigation

The first medical event of significance to this litigation occurred on the night of 4 September 1995 when Kurt collapsed at home. His father had come home from work early that day. He described the events in the following exchange with counsel: “Q. I want to take you to a situation on this day. Can you remember seeing Kurt dressed otherwise than you would have expected? A. Yes. Q. What was he in? A. Kurt was in his pyjamas. Q. Did he say anything about how he was? A. He told me he hadn’t been feeling well all afternoon. … Q. Did you commence to prepare the evening meal with Kurt and Annika sitting at the table in the kitchen, was it? A. Yes. Q. Watching television and talking? A. The house we were living in at that stage, the kitchen had a small room off it like a meals room which, of a night, the kids would be in. There was a round table. We still have the table. There was a television in the corner. While I was preparing the meal, the children, Annika and Kurt, were sitting at the table. When I say “preparing the meal.” I was warming up something that Jan had pre-prepared. Q. I want you to describe in detail what happened, Mr Halverson… A. Okay. The meal was simply lasagne, quite easy to warm up and serve. Both the kids were sitting at the table. The table was on my right, from the kitchen, and Kurt was on the left of the table and Annika on the right, both half facing the television and watching the television. I gave them the meal and I sat between them. The kids had been sitting there five to ten minutes, which was fairly long for Kurt, but he hadn’t been feeling well, because he didn’t sit still a great deal, for a long time. We had been eating the meal for a while – I can’t determine how long – and Kurt fell forward. He slumped forward and his face went into his food. He fell forward with his face in his food and then he fell off the chair towards me on to my side. He fell on his side and he had food on his face. I cleaned the food off his face, but he was unconscious the whole time, but he was breathing. Q. Was he making any movement? A. None at all. He was just quite still. I cleaned the stuff off his face, and when he came around, when he started to wake up, I started to lift him up so that he was sitting on the floor, but up, and he was groggy and he was a little bit aggressive, in the sense that he didn’t want me touching him or helping him, but he was groggy. Q. How long did he appear to be unconscious? A. I’d say it would be about 30 seconds… Q. After he came around, did you have any discussion with him as regards any recollection he had of the event? A. I asked him the logical questions, that being what happened, is he all right? Kurt didn’t really know what I was asking or why he was on the floor. Then I realised he didn’t – he hadn’t been aware of what happened to him.”

The relevant medical records show that Kurt was taken into Cessnock Hospital that night and was seen by the defendant. Dr Dobler’s notes record a “possible fit tonight” and flag the possibility of a viral illness. The notes show that Dr Dobler auscultated Kurt’s heart and that it was making the normal sounds. There was no murmur detected. Dr Dobler ordered some tests to be carried out. The results indicated a reduction in white blood cells consistent with a viral illness. Prolactin levels are known to increase after an epileptic seizure, and Kurt’s levels were high. This suggested to Dr Dobler that the possibility that the incident was the result of a seizure should be further investigated.

Mr and Mrs Halverson later consulted Dr Dobler in relation to this incident. According to Mr Halverson, they were told by the defendant that he was of the opinion that Kurt had suffered a petit mal but not an epileptic fit. Mrs Halverson had previously been diagnosed with epilepsy and they were concerned that Kurt had the same condition. Mr Halverson said that: “What he described was a petit mal was like a short sleep and he said that it was not uncommon for young children to experience that and that it was – school teachers of young children saw it happen; once again, it was not uncommon for school teachers of young children to see that within their class. He also went on to tell us that, despite that, he would like to investigate it further, and he suggested two things. He suggested that Kurt go to the John Hunter Hospital for an EEG and he suggested that that be backed up, or once that EEG happened, that Kurt was to see a paediatric neurologist, Dr Ian Wilkinson, whose rooms were in Lambton.”

Dr Dobler referred Kurt for an EEG, which was performed in the Clinical Neurophysiology Unit at John Hunter Hospital on 24 October 1995. The report for that EEG contains a brief history which records, inter alia: “Epileptic fit. ? complex partial seizure. Serum prolactin increased + afterwards. Mother has TLE [temporal lobe epilepsy].” The report ends: “Clinical interpretation: This is a normal report.”

Dr Dobler also referred Kurt to Dr Wilkinson, a specialist neurologist. In his referral letter, Dr Dobler described Kurt’s “turn” as an “episode which was not typical of a grand mal seizure but which I thought may have been a complex partial seizure.” In his evidence Dr Dobler described a complex partial seizure as one that does not involve generalised jerking, but which may involve some abnormal movement. Dr Dobler described the event itself as involving Kurt “sitting at the dining table when he became non communicative and then started with some unusual movements which were not violent.” Mr Halverson did not agree that Dr Dobler had been told that Kurt became non communicative, nor did he accept that Kurt had displayed any “unusual movements” other than falling face-first into his food. The differences may be explained by the fact that Dr Dobler wrote the referral letter from memory almost four months after the incident.

Dr Wilkinson sent Dr Dobler a letter in respect of his consultation with Kurt in which he states: “The presenting problem is of an event that took place recently, when he had been generally unwell through the day. It sounds as though it might have been a viral illness, and he was off his food. His father made him some lasagne, which he normally liked very much, and he was sitting down to eat it about 7:30 pm, when he felt that it tasted unpleasant, and at that stage he looked very pale, and his head slumped forward, and he fell out of his chair. He was on the ground briefly for about 30 seconds or so, and there was no stiffness or jerking. He woke a bit confused, and he had a bit of a headache. He had been vomiting through the day. … His had [sic] never had a past history of fainting or seizures, and there is no family history of fainting. His mother has a history of temporal lobe epilepsy since 32 years of age. There is really nothing in the past history that appears to constitute a hazard to his neurological development. … In the presence of the normal EEG, with an event that really sounded as though it could have been a faint, I would be inclined to think of this as a faint and not a fit. I think that elevated prolactin levels can occur in other events that can lead to unconsciousness, but do not have to be actually convulsions…. The family history of temporal lobe epilepsy in his mother is also not a terribly strong point, as temporal lobe epilepsy is usually not inherited. I think we should regard this as being a faint, not a fit, and consider it a one-off. If he does have further events that are not related to situations that might produce a faint, then it would be worthwhile repeating his EEG, but I think we should get it done with him asleep, and that would probably require sleep deprivation.”

At this time it was noted that Kurt’s blood pressure was about 120/60 when lying down, and that it fell to about 80 systolic when he stood suddenly. Dr Dobler said in his evidence that this “suggested that Kurt may be predisposed to episodes of postural hypotension.” Dr Wilkinson also noted that Kurt had a hand tremor and referred him to the Paediatric Occupational Therapy Unit at John Hunter Hospital.

With respect to the differing recollections of Mr Halverson and the defendant I am completely satisfied that Mr Halverson’s recollection is accurate. His account of Kurt falling into his food is consistent with Dr Wilkinson’s note that “his head slumped forward” before he collapsed to the floor. Although the matter was the subject of some discussion by various of the doctors who gave evidence I do not believe anything turns on the report that his food tasted unpleasant. Whatever else was occurring, Kurt was ill and had lost his appetite. In these circumstances his food was not likely to taste as pleasant as it normally would.

In cross-examination, Dr Dobler stated that he regarded Dr Wilkinson’s use of the word “faint” in his letter as a specific diagnosis of vasovagal syncope. The following exchange occurred: “Q. Do you say, doctor, that you relied in any way on the wording in Dr Wilkinson’s report where he said words to the effect that it should be regarded as a faint, not a fit – A. Yes. Q. – which still left you with a syncopal event, didn’t it? A. A single syncopal event, yes. Q. Undiagnosed. A. Diagnosed as a faint. Q. But that’s a syncope, isn’t it? A. A faint is a syncope, but a faint is a specific diagnosis. Q. Well, doctor, that, I suggest to you, is a very highly contentious proposition in the context of what is being reported on here. A. Sorry, is that a question? Q. Yes, it was a question, but it’s probably argumentative and I shall not pursue it. What I do put to you is this, that clearly what the neurologist is saying is that it’s a loss of consciousness which is not epileptiform in origin. A. He’s saying that, yes. … Q. There is no diagnosis as to what caused the loss of consciousness. A. I don’t believe that is true. Diagnosed “faint.” HIS HONOUR: Q. What I’m not sure about is whether, in the ordinary course, having diagnosed, as you say, faint, you would go further and look for the cause of the faint? A. My understanding, from the description that Dr Wilkinson is giving, is that he’s using the word “faint” to signify a vasovagal event. Q. Where does that come from? A. They’re commonly interchangeable terms, although – and the fact that he suggests that should further episodes occur, further neurological investigation occur, rather than anything else. Q. So, in my layman’s language, the faint has been caused by vasovagal indicia? A. That’s correct. … Q. You accepted from what he told you, did you, that he has diagnosed a vasovagal turn? A. That was my understanding from the letter. Q. Did you call him up and ask for clarification of this? A. No, I did not. Q. This terminology – if you look at the article in Murtagh, it’s specifically called “Faints, fits and funny turns,” isn’t it? A. That’s the heading of the article. Q. And it’s all about how you get to a diagnosis for anything that comes under those headings? A. Yes, it is. Q. And Dr Wilkinson hasn’t told you what was the cause of this faint in his letter, has he? A. No. Q. Did you take comfort at the time in his observation that you could regard it as a one-off – as non-epileptiform, as a faint and a one-off? A. Yes. Q. Did you take comfort from that? A. Yes. … Q. Dr Dobler, I don’t mean to be aggressive, but I’m obliged to put to you that your protestation that “faint” is a diagnosis is a nonsense. A. Sir, if you could read further in Dr Wilkinson’s letter, “if he does have further events that are not related to situations that might produce a faint” – this is highly suggestive to me that Dr Wilkinson believes this is vasovagal, such that there is a precipitating event that caused the faint. Q. Doctor, I don’t want to argue with you, but where does he use the word “vasovagal”? A. He does not use that word. Q. And you know, I suggest, full well that if that was his diagnosis, he would have said so. A. I am not aware of what he would or would not have done.”

Five cardiologists were called in the trial, although one of them – Dr Silberberg – was called as a witness of fact. He gave evidence separately. The four other cardiologists, Professors Harris and Saul and Associate Professors McGuire and Richards, gave evidence concurrently. I have provided a description of the qualifications and expertise of the cardiologists later in these reasons. In this judgment, a reference to “the cardiologists” is a reference to the four cardiologists who gave concurrent evidence, but not to Dr Silberberg, unless the context indicates otherwise. The cardiologists gave consideration to whether Dr Wilkinson had diagnosed a vasovagal faint. When giving their evidence the following exchange occurred: “PROF HARRIS: It is the third paragraph on Page 54, your Honour, the end of the first sentence: I would be inclined to think of this as a faint, not a fit. To me often, in these circumstances, it is as good a diagnosis as you get. HIS HONOUR: Does that mean that, as you understand it, he is saying, by referring to it as a faint, that it does not have a cardiac connection? PROF HARRIS: Yes, that he considers this to be either vasovagal or hypotension. That would be my interpretation if I were to receive that letter. HIS HONOUR: Can I ask each of the other Professors – would you interpret the letter in that way or differently?… PROF MCGUIRE: I accept that Dr Wilkinson intended to convey the diagnosis of a faint or hypotensive episode, not an arrhythmia. If he’d thought it was an arrhythmia, he would have referred the patient for investigation. HIS HONOUR: Professor Richards? PROF RICHARDS: Dr Wilkinson writes: I think we should regard this as being a faint not a fit and consider it a one-off. If he does have further events that are not related to situations that might produce a faint, then it would be worthwhile repeating his EEG, but I think we should get that done with him asleep. At that stage, Dr Wilkinson does not address the possibility that it could be anything other than a faint or neurological problem. Because fainting is diagnosed by exclusion of other diagnoses, it is my view that this is simply the view of a neurologist that it was not a fit and he thought it was probably a faint based on the description that he gave of the event. But I don’t really think it establishes a diagnosis of vasovagal syncope or hypotension against a cardiac diagnosis of an arrhythmia. … HIS HONOUR: What would you [Professor Saul] tell me? PROF SAUL: Again, I think being a paediatrician is an advantage in interpreting such a letter. To a paediatric neurologist every syncopal event is a fit or a faint and exactly as Professor Richards said, all he is saying here is that it wasn’t a fit. In every other kind of faint, we have used the word “faint” to mean benign and non-cardiac. A neurologist just means it’s not a fit and there is a great book by John Stephenson from Glasgow who is a quite famous paediatric neurologist who is an expert on fits and faints, and that’s the name of his book, and many of the faints in his book are arrhythmia based, bradyarrhythmias and tachyarrhythmias and other things, and they are all considered faints, whereas the fits are the seizure disorders. So a paediatric neurologist by saying this simply means that, “It’s not me, it’s not my area, and everything else is a faint.” Then the question came up, should he or could he have referred them to a paediatric cardiologist? That really depends on the neurologist how they deal with it. He didn’t recommend it back to the doctor, but he also is dealing with a GP who he assumes has his own evaluation of what was going on and would carry on the evaluation possibly in some other way. I don’t think in any way we can interpret this as saying that the neurologist has cleared him and he certainly doesn’t say anywhere in the letter that he thinks this is vasovagal syncope. PROF MCGUIRE: Phil, the training system in Australia is a little bit different from the training system in the United States. All specialist physicians in Australia train in internal medicine before they specialise. We don’t go straight from being an intern or a resident to a specialty. We all train in internal medicine. So this doctor is trained in special medicine. Don’t you think if he’d thought an arrhythmia was a likely possibility, he would have referred the patient on? PROF SAUL: Except he sees paediatric patients, so he doesn’t think about arrhythmias very much. The whole problem here in the entire case is that nobody thought of arrhythmia. Even when this boy was admitted to the hospital for two days because of a syncopal event, nobody got an EKG and put him on monitoring…I don’t know how to explain what the neurologist says other than that I can’t identify this as being that he is saying that it is not an arrhythmia. HIS HONOUR: Professor Harris, I think you started this discussion – I will ask Mr Higgs in a moment – but do you want to respond. PROF HARRIS: I am not a paediatrician, but I can merely saying [sic] that in my experience neurologists feel comfortable make [sic] a diagnosis of simple faints. They are very attuned to the possibility that patients have a cardiac basis for syncope and they don’t hesitate to refer either back to the GP suggesting cardiological consultation or it’s referred directly to a cardiologist because of the general seriousness of the problem, if they believe there is a cardiac basis. I think it is projecting too much into Dr Wilkinson’s mind to suggest that in saying it was a faint he was including every possible cause, including an arrhythmia. My interpretation of the letter was that he had made a specific diagnosis.”

The plaintiff submitted that because the defendant failed to offer an explanation for not calling Dr Wilkinson as a witness, I should infer that nothing he would have said on this issue would have assisted the defendant’s case: Jones v Dunkel (1958) 101 CLR 298. At the end of the exchange between the cardiologists I am left in doubt as to whether Dr Wilkinson’s words can be taken as far as Dr Dobler contended. It seems clear that Dr Wilkinson was excluding neurological causes (such as epilepsy) as being responsible for Kurt’s syncopal event when he says “we should regard this as being a faint, not a fit,” but whether he was also excluding the possibility that Kurt’s faint had a cardiological cause is uncertain. Without hearing from Dr Wilkinson a certain finding is not possible. However, I have ultimately concluded that the resolution of this issue is not material to my ultimate conclusions in the proceedings.

Kurt turned fifteen on 25 September 1997. Shortly before this date he had begun to complain of unusual symptoms, including feelings of déjà vu. His father recounted that Kurt had said “that he felt like he was being there but not there.” Kurt first told Dr Dobler about these symptoms at a consultation on 29 August 1997. Dr Dobler’s notes for that day record, inter alia, “Episodes of light-headedness followed by nausea. Dream like state at beginning.” Dr Dobler organised a sleep-deprived EEG on 23 September 1997 which was normal and revealed no epileptiform activity. Like the first EEG, this indicated that Kurt’s previous syncopal episode was unlikely to have a neurological origin.

Although his neurological tests were normal, Kurt continued to suffer from severe headaches. The defendant diagnosed migraine headaches and he prescribed Imigran. Originally this was taken orally but later it was delivered through a nasal spray, which proved to be much more effective treatment. 29 June 1998 – collapse outside Dr Dobler’s surgery

On the morning of 29 June 1998 Kurt was quite unwell. He stayed home from school and was cared for by his grandmother at his grandparents’ home until his grandfather (Mr Ron Halverson) had returned from attending to his horses. Mr Ron Halverson gave the following evidence of the events which followed: “Q. When you got home from the stables, did your wife ask you to take Kurt to see Dr Dobler? A. Yes. Q. Did you contact the surgery and organise an appointment? A. Yes. Q. Having done that, did you take Kurt in your vehicle to see Dr Dobler on that Monday morning? A. Yes, I did. Q. As you were travelling to that appointment, did you note something about Kurt’s appearance? A. Kurt had lost all the natural colour on his face at that stage and he was very grey. Q. When you got to the surgery, did you drive up the back lane to the surgery and stop in the car park at the back, as opposed to going in the main entrance on the street? A. Yes, I did. … Q. When you reached that point that’s marked on exhibit D, the sketch plan, what happened? A. I was assisting Kurt down the path at that stage. Q. Did he say something to you? A. Yes. He had his hand on my shoulder. I was assisting, with my hand under his arm and he had his hand on my shoulder, and he said, “Pop, I think I’m going to faint,” and I said, “Hang on, mate. I think you’ll be all right,” and with that, he did; he collapsed. Q. Did you lose your grip on him, or what happened? A. No, I grabbed him more solidly and I eased him to the ground. Q. You eased him to the ground? A. Yes. Q. …He was eased down on to the ground, and what did you see when you looked at him? A. I was talking to him and he never answered me, so he was in a state of unconsciousness. I eased him. Q. So what did you do? A. I eased his left hand under his head to lift his head up a little bit and I checked his tongue, as far as possible, and I ran as fast as I could into the surgery to get assistance. Q. What did you do when you got inside the surgery? A. I called out at the desk and said I wanted to see the doctor immediately, that Kurt had collapsed outside. Q. At the desk, was there anyone attending there? A. Yes. There was a girl behind the desk and Jill Dobler was in attendance there, too. … Q. You personally recognised Jill Dobler? A. Yes. … Q. What was the state of the surgery? A. Oh, the surgery was very full at the time. Q. What happened after you had called out that you needed a doctor immediately? A. I went back outside to Kurt as quickly as possible, and Jill Dobler followed me out. Q. Obviously, you went to where Kurt was. A. I did. Q. What happened there? A. At that stage, Kurt was starting to regain consciousness. I spoke to him and he answered me. Mrs Dobler and I got him to his feet, took him round to the back of the surgery and took him into the treatment room. Q. I think Dr Dobler came immediately to see him? A. Yes. Mrs Dobler went to the door. I think Dr Dobler had a patient in there. Mrs Dobler went to the door, and Dr Dobler came out immediately. Q. What happened then? What do you recall? A. Well, Dr Dobler went to Kurt. I can’t remember what he did or anything else, but he was talking to Kurt and then he questioned me thoroughly as to what happened. … Q. You say that Dr Dobler questioned you thoroughly as to what happened? A. Yes. Q. What did you tell Dr Dobler? A. I told him that Kurt had been dropped off to us that morning and Lois had asked me to take him in there; he was sick and possibly had nausea; I hadn’t seen him vomit, but Lois had a bucket out in the bedroom when I was there; and that I brought him in and he collapsed going down the path and was unconscious when I left him. Q. Did you stay on for some time at the surgery? A. Yes, quite some time. Q. In the course of that, did your daughter, who worked at the Cessnock Council, come down – did anyone else turn up while you were there? A. Yes, my daughter and her husband, Maurice Kidd, turned up in their lunch hour from the council.”

Both Dr Dobler and Mrs Dobler (who worked in her husband’s surgery and who is a qualified nursing sister) gave evidence. Neither of them recall being told that Kurt had collapsed and Dr Dober’s clinical note is confined to one word “migraine.” Mrs Dobler stated that if she had been told of the collapse of a patient she would have instituted particular procedures to care for the patient and seek competent advice. She does not remember initiating these procedures in relation to Kurt.

I accept Mr Ron Halverson’s evidence. His account of the relevant events was completely convincing. I intend no criticism of Dr Dobler or Mrs Dobler but I am satisfied that with the exigencies of a busy practice (the surgery was full at the time), the particular events were not marked in their memories. I have no doubt that Mr Halverson told the defendant that Kurt had collapsed and that he was very unwell. However, whether the doctor appreciated the full extent of the information he was given seems unlikely. Given the symptoms which I am satisfied were reported to him, a one word note of “migraine” was an inadequate clinical record. Having been told, as in my view he was, that Kurt had collapsed, this should have been recorded and consideration given to the contribution this knowledge could make to a possible diagnosis. I appreciate that to this point Kurt had presented with significant problems with migraine headaches and a headache was reported on this occasion. Understandably, having regard to his history, Dr Dobler would be likely to have assumed that the latest event was confined to being another migraine. Notwithstanding this conclusion, the notes should have made some reference to the circumstances of Kurt’s presentation. The failure to do so indicates that – at least at this point in time – Dr Dobler gave very little, if any, consideration to the potentially sinister nature of recurrent syncope.

Kurt spent some time in the treatment room at the surgery. This was unusual. He was visited there by his uncle and aunt who took time from their work to come to the surgery. They confirmed that Kurt was seriously unwell on this day. However, he was allowed to return to his grandparents’ home. This surprised his grandmother. He had appeared so ill that she thought he would end up in hospital.

Later that day, Kurt was taken to Cessnock Hospital by his parents. He was seen there by Dr Dobler, who was a Visiting Medical Officer at the hospital. The hospital notes made by Dr Dobler were not much more detailed than the records kept in respect of Kurt’s visit to the surgery earlier that day. The presenting symptoms were listed simply as “Migraine, vomiting, afebrile.” Other information, such as blood pressure and drugs administered, is also recorded. Dr Dobler gave evidence that – in respect of both the notes from his surgery and the hospital notes – it would have been his usual practice to record that the patient had lost consciousness earlier that day if the patient had in fact told him that this was the case. For the reasons given above, I do not accept that this was the case in this instance. In notes taken by nursing staff, it is recorded that Kurt is allergic to MSG and that the headache and vomiting had started after he had eaten a sausage roll the day before. There is no mention of Kurt having lost consciousness earlier that day in these notes. Kurt was discharged from hospital the following day.

Kurt’s migraines continued. After a consultation on 25 January 1999, Dr Dobler referred him to Dr Katekar (a neurologist) in relation to his migraines, and to Dr Loblay in relation to possible food allergies. Most of the correspondence from Dr Katekar relates to the use of the medication Sandomigran, which Kurt had been taking since January. It is repeatedly noted that the medication was effective at controlling Kurt’s migraines to some extent, but that there were concerns about side-effects such as drowsiness and lethargy. Correspondence from Dr Loblay to Dr Dobler indicates that Kurt’s migraines might have been triggered by ingestion of biogenic amines and MSG, and that avoidance of these foods had resulted in Kurt’s headaches diminishing in intensity.

I consider the significance, if any, of the 29 June 1998 syncopal event later in these reasons. The events of February 2001 1 February 2001 – a heart murmur is found

Kurt continued to suffer from migraines. One night towards the end of January 2001 his symptoms were particularly acute. He complained to his father of headache and nausea and was vomiting. Kurt’s nasal Imigran was not effective. Even after waiting two hours and taking a second dose, his symptoms only seemed to get worse. Reluctant to move Kurt when his symptoms were so severe, Mr Halverson contacted Dr Dobler and asked him to make a house call. Dr Dobler was on duty at Cessnock Hospital at the time and could not get away, but he asked Mr Halverson to come and see him. He gave Mr Halverson some Imigran to administer by injection. Mr Halverson returned home and gave Kurt the injection. His symptoms cleared within 30 minutes. However, Kurt did not recover well from this incident, and the next day he was tired and lethargic. Kurt was concerned about the severity of the incident and an appointment was arranged with Dr Dobler on 1 February 2001.

At the appointment Dr Dobler conducted a physical examination of Kurt which included auscultation of his heart. He reported a murmur. Dr Dobler’s notes state “noted to have a mitral type murmur – arrange for CXR [chest x-ray].” The murmur is described as “2/6 Pansystolic murmur radiating to axilla.” Dr Dobler gave evidence of this consultation. The following exchange occurred when he gave evidence-in-chief: “Q. Sir, before the luncheon adjournment, I was asking you about the consultation of 1 February 2001 and, in particular, referable to your note on page 6 of exhibit G. Do you have that open? A. Yes, I do. Q. In relation to the heart examination that gave rise to your note referring to mitral-type murmur, that involved, did it, the use of a stethoscope listening to the patient's heart? A. That is correct. … Q. And the "heart sounds times 2", what does that mean? A. It means that there was a first and second heart sound and no other heart sounds. Q. The "murmur 2/6" - I think you've told us that that calibrates how strong or loud or soft the murmur was? A. That's correct. Q. How do you give it that score? What's the softest, what's the loudest? A. The softest is 1 on 6, which would be barely audible, through to 6 on 6, which could be palpated by having just a hand on the chest. Q. Before the luncheon adjournment, you gave a description of what it was that you heard. You referred to a sound from the axilla, if I recall correctly. I'll just bring it up on the screen. You could hear an extra noise, which was maximal at the lower left sternum. What was the extra noise that you heard? Was that the murmur? A. The murmur, yes. Q. In respect of the normal two sounds that you hear, is the murmur the extra sound in addition to those two normal sounds that you referred to earlier on? A. That is correct. … Q. You said that the extra noise was maximal in the lower-left sternum. What do you mean by that? A. The standard areas for listening to the heart would be the upper-left sternum and the lower-left sternum, across towards the nipple at the apex, and then guided by any extra sounds, you may examine then the carotid arteries and then up into the axilla. Q. The murmur also at the axilla - where is that? A. Basically, at the front of the armpit. … Q. The murmur being described as "pansystolic", what did you mean to convey by that? A. It meant that I could hear it from the very start of the - directly from the first heart sound throughout, ceasing with the second heart sound. Q. Is there another type of murmur? A. There's an ejection systolic, which tends to start slightly after the first heart sound and finish slightly before the second heart sound. There are also diastolic murmurs, which occur in the interval between the second heart sound and the following first heart sound. Q. With a murmur that attracts a score of 2 out of 6 in the way that you've been over, is there difficulty in differentiating between, say, for example, whether it truly is pansystolic as opposed to, is it, systolic ejection? A. Yes. At 2 on 6, it's a relatively soft murmur, so it would be quite difficult to ascertain with absolute certainty. Q. At the time, what was your understanding as to the implications of this finding, this murmur, in the context of this examination? A. Having ascertained that I couldn't see any evidence of acute infection within the heart, so-called endocarditis, and that I could detect no evidence of cardiac failure, I believe that the most likely was that this was an innocent murmur, possibly associated with a viral illness. Q. When you say "an innocent murmur", can you give us an idea, in the context of someone presenting with a complaint of fatigue, lethargy, that type, how common or uncommon this type of finding is? A. In a young person, it is not uncommon to detect a cardiac murmur in a febrile or a viral illness because the body's metabolic rate tends to go up, and that hyperdynamic state often causes you to hear a murmur despite the fact that there are no structural abnormalities of the heart. … Q. And, as you understand it - I don't think it's controversial - with illness, sometimes you can hear a murmur that simply is a reflection of the blood going through the heart at a different speed, and the murmur is a reflection of simply a turbulence or agitation of the blood within the chamber of the heart; is that a fair layman's description? A. Yes, that's correct. Q. Do you recall coming to the view that it was, in all likelihood, an innocent murmur in these circumstances, or are you just working on usual practice? A. I believe at the time that I had a recollection that I had excluded what I thought were conditions which required urgent treatment, and it would be then my usual practice to arrange some investigation but then to review the murmur at some stage later.”

A chest x-ray was arranged so as to exclude the possibility that the murmur was caused by endocarditis or myocarditis. Kurt had the chest x-ray the following day (2 February 2001). In a report written on the same day the radiologist, Dr Mackley, stated that: “The lungs are clear. The heart, hila regions and pleural surfaces appear normal. The history of heart murmur noted.”

Kurt continued to remain unwell. 4 February 2001 – Kurt collapses again

The events of 4 February 2001 are an important part of Kurt’s medical history. Kurt collapsed at home. His father’s account of those events was given in the following exchange: “Q. On the Sunday…did you note what Kurt was doing most of the time? A. On that Sunday, he laid around the house and watched television just about all day. Q. Did he say anything about how he was feeling? A. I asked him, of course, and he just told me he didn’t feel like doing anything and didn’t really feel the inspiration or energy to do anything. Q. That night, Sunday, 4 February, who was home? A. Jan, Annika, Kurt and myself. Q. Do you remember being in the kitchen with Kurt? A. I remember Kurt being in the kitchen. He came out to get a glass of milk and I was in the dining room – Q. Just stop there, please. When you say you remember him being in the kitchen and he came out – came out from where? A. Came out from his bedroom. I had been in the lounge room and I went to check on Kurt, and as I got in to the dining room, which was between the kitchen and the lounge room, he walked out of the doorway which would have led to his room and said he was just coming to get a glass of milk. … Q. He came out of his room, and what did he do? A. Kurt came out of the room. He saw me standing in the dining room. I was walking – I was on my way to see him, and he told me he was coming to get a glass of milk, and then instead of doing that immediately he jumped up on the stool at the end of the bench. Q. Yes, and what did he do? A. He was just talking to me, having a conversation. … Q. So what did he do after he sat on that stool and commenced talking with you? A. He talked to me for a few minutes and then, while continuing to talk, he got up from his stool to get himself a glass of milk, and got himself a glass of milk. Q. Can you describe in detail…what he did? A. Certainly. Kurt got up from the stool…and went to the refrigerator…He opened the refrigerator, took out the milk. Kurt got [a] glass out of the cupboard, put it on the bench, poured the milk, turned and put the milk back in the refrigerator, went back, picked up his glass, walked over to the stool, put his glass of milk on the bench and sat on the stool. Q. Did you see him do anything after he sat on the stool? A. As I said previously, Kurt had continued to talk the whole time, so I was pretty well just standing in the dining room listening, as you do with your children, and when Kurt lifted the glass up and started to drink, I – Q. Yes, what did you do? A. I started to turn back to go into the lounge room…but as I did, as I started to turn, Kurt called my name. Q. What did he say? A. He said, “Dad.” Q. What happened? A. He just called my name, “Dad,” and I turned back and Kurt had the glass near his mouth but I saw he had sat up very straight. He put the glass down and then slumped. He sort of just jellied and started to fall off the stool. Q. What did you do? A. Because I had turned – luckily, because I had started to turn towards him, I could catch him before he hit the floor, and I laid Kurt on to the floor and he was – he was totally still and loose, and I called for Jan and her and Annika came in. Q. Just pause there. Did he appear to be conscious or unconscious? A. He had his eyes closed and he was unconscious but breathing. Q. Was he moving at all? A. Not at all. Q. Any jerking or anything like that? A. He was not moving at all. Q. For how long did he appear to remain unconscious? A. He would have been unconscious over 20 seconds. But to define the upper limit, he would have been unconscious for quite a bit shorter than a minute. … Q. Once again, Mr Halverson, when Kurt regained consciousness, did you question him, ask him if he was all right? A. Yes. The obvious but stupid question is, “What happened?” Q. You asked him what happened? A. Yes. Q. What did he say? A. I don’t think he answered me. I can’t recall a direct answer, but I ended up asking, “are you all right?” Jan came in and was questioning him as well, and Kurt said he couldn’t answer us; he didn’t know what had happened because he knew he was lying on the floor, we were all sitting around him. He was more or less asking us what happened. Q. So did you and your wife immediately take him to the emergency department at Cessnock? A. Yes. Q. Do you remember his being seen by a doctor you know as Dr Anne Wakatama? A. Yes. Q. Did you tell her your understanding that Dr Dobler had detected a heart murmur several days earlier? A. Yes. Anne asked me a lot of questions. I told her Kurt hadn’t been well and that he had seen Dr Dobler on the Thursday and what had been detected, and I explained to her what had happened that evening.”

Kurt arrived at the hospital at 9:25pm. At that time, a triage nurse wrote down Kurt’s presenting symptoms. The record reads as follows: “Walked into ED [Emergency Department] with parents with H/O [history of] ?? [possible] seizure this pm lasting approximately 20 seconds. Parents state patient has a P/H [prior history] of migraine headache 1/52 [one week] ago. F/B. Lethargy +++ [i.e. extreme lethargy]; has seen m.o. [medical officer] re same ?? viral illness; also has [high] temps. Tonight stiffening of limbs and ? loss of colour for approximately 20 seconds at home. GCS [Glasgow coma score] 15/15 O/A [i.e. fully conscious on arrival]. Pupils = reacting briskly. Patient alert, looks unwell, ? pale.”

Dr Wakatama attended Kurt at 10:00pm. She noted the following history: “Has been unwell with lethargy and fevers. Saw GP 2/7 [2 days] ago – provisional diagnosis viral illness. Has remained unwell. Tonight got up to get a drink of milk and felt dizzy and ? fainted. Father caught him and he had some stiffening of limbs and then went limp. LOC [loss of consciousness] 30 seconds. OE [on examination]: alert and orientated, not post ictal [i.e. not drowsy and combative if roused], no neck stiffness, sweaty, chest clear, ENT NAD [ear, nose and throat – no abnormality detected]. PD [provisional diagnosis]: viral illness with faints, but need to observe for seizures.”

Dr Wakatama also ordered blood tests. She has no independent recollection of her consultation with Kurt. She gave evidence that when she wrote “chest clear” in the hospital notes, it would have been her usual practice to “auscultate his chest, to listen to his breath sounds and I would listen to his heart, to check for his heart sounds and to check if there were any added sounds there.” Her notes implied to her that she could not hear a murmur, although usually she would make a note of whether there was or was not a murmur.

Kurt was admitted at 10:50pm. The admission sheet was filled out by a registered nurse. Under the heading “Past medical history,” the nurse has recorded “Temp Sweats [for] 3 days with lethargy. Migraines – last one last Saturday. Headaches, swollen gland back of head. [Left] and [right] side.” Under “Current medical conditions,” it says “Temp – sweats lethargy. Dizzy past 3 days tonight fainted ? Fitted at home [indecipherable] approx 20 seconds. Eyes open. Back and neck stiffened then slumped.” At around the same time the same nurse recorded the history of Kurt’s illness in more detail in his “History, Examination and Progress Report.” It relevantly states: “Nursing. New admission B Ward 2250. Wheeled into ward on chair by wardsman, accompanied by mother. Mother (Jan) staying in overnight. P/H migraines. On Sandomigran. Has been unwell last 2-3 days with temps, sweats, lethargy and dizziness. Got up tonight (not quick) to get drink of milk. Whilst drinking milk felt dizzy has no further memory until woke up. Father told mother that when Kurt was drinking milk his eyes were open his neck and back stiffened then he slumped. LOC approx 20 seconds. Kurt stated he has been having déjà vu lately. Mother has history of epilepsy. Kurt has allergy to amines in food [which lead to] migraines.” Kurt stayed in Hospital overnight. The events of 5 February 2001 and subsequent days – Kurt has glandular fever

Dr Dobler saw Kurt in Hospital on 5 February 2001 when he was doing his scheduled rounds. He performed an examination of him. His notes read: “Syncopal episode with seizure on the background of viraemic symptoms. Pulse 80, afebrile.” A symbol then appears which Dr Dobler interpreted as meaning that a chest examination was clear. He notes that Kurt’s abdomen was soft and non-tender and that there was “no neck stiffness.” Dr Dobler cannot specifically recall the chest examination, but his usual practice would involve sounding the patient’s heart with a stethoscope. If nothing (such as a heart murmur) was detected Dr Dobler said that he may not record this in his notes, although it would be unusual for this to occur. Kurt’s prolactin levels were checked but the results (which were available on 6 February) were in the normal range, indicating that Kurt’s syncopal episode was not an epileptic seizure.

Dr Dobler saw Kurt again on the same day after having had access to the results of the blood tests ordered by Dr Wakatama the night before. Those results led Dr Dobler to positively diagnose Kurt as suffering from glandular fever. Dr Dobler’s notes state “Glandular fever. May go home. Repeat bloods at the end of the week.” He was discharged that day.

Ms Megan McKay, Kurt’s girlfriend at the time, was present when Dr Dobler saw Kurt at the hospital. Although she had some difficulty identifying the time Kurt was discharged, Ms McKay recalls being with Kurt at the time. She gave the following account of her observations that afternoon: “Q. And did you stay with Kurt and Dr Dobler? A. Yes. Q. Did you witness a conversation between them? A. Yes. Q. Could you, doing the best you can, relate what was said by whom and what was said in reply? A. Yes. Dr Dobler told Kurt that he was free to go home and that he was being discharged. Kurt said, “Are you sure that’s okay? You mentioned something about a heart murmur before.” And Dr Dobler said, “No, that’s not a big problem, nothing to worry about. You can go home.”

I accept her evidence.

On Tuesday (6 February) Kurt’s condition was stable. He was not getting any better but his condition was not deteriorating.

When Mr Halverson got home from work on Wednesday Kurt had been vomiting. He looked dehydrated. Mr Halverson again took him to hospital. The triage nurse reported Kurt’s symptoms as follows: “Presented to A&E [accident and emergency] in c/o [company of] father who states patient was discharged from BW [B Ward] Sunday [sic – Monday?] and has had nausea today and father is concerned patient is becoming dehydrated.” On the same form Dr David Outridge made the following notes in relation to Kurt: “Readmitted with glandular fever. Concentrated urine. Allergies – nil. On examination, red throat, tongue coated. Examination of the abdomen indicating tenderness of the upper abdomen. Treatment – intravenous fluid, nil stat, oral Phenergan.” Dr Dobler referred to these notes when he saw Kurt in hospital the next day.

Dr Dobler’s clinical notes for 8 February 2001 state: “Somewhat unwell. Possible jaundice. Fever overnight. Proteinuria for repeat bloods, 24-hour urine, urinary red blood cell morphology. Mid-stream urine examination. Note: one positive blood culture. Start IV, Keflin.” “Proteinuria” refers to the presence of protein being detected in Kurt’s urine following a dipstick test. The result was consistent with Kurt’s continued viral illness. Other tests gave results consistent with glandular fever. Kurt also returned a positive blood culture, which indicates that he had bacteria growing in his bloodstream. Dr Dobler said of his treatment of Kurt that day: “Q. In relation to the 8th, when you saw him, do you have a recollection of any of the examinations that you carried out? A. Yes. I was cognisant of the fact that he’d had a positive blood culture and, with that in mind, I have a recollection of performing a full examination of him, including heart, chest and abdomen, the purpose of which is that – he had previously had a murmur and the implication of having a murmur as well as a positive blood culture raises the distinct possibility of bacterial endocarditis. So I was careful to look at that and make sure that that was not the case. Q. When you go to your note on page 94 in respect of the examination, is there any note there referrable to your recollection of that examination being carried out? A. There is not. … Q. So you’re going on recollection, but there’s no note of it? A. That’s correct. Q. How does that fit in with usual practice? A. It’s not common, but it occasionally occurs when performing an examination and I just write my conclusions rather than noting the entirety of the examination. … HIS HONOUR: You say on page 94 there’s your note of what you did, but can you explain to me what you say you did beyond that? A. Beyond that I recall performing a general physical examination. Q. Just explain to me what that means you did. A. It means that I would have examined the patient’s throat, had a look at his eyes, palpated his abdomen, listened to his chest and [auscultated] his heart, as well as looking for other signs of endocarditis. … Q. When you say you looked for other signs of bacterial endocarditis, what did you do to look for those things? A. I had a look at the patient’s hands and the nails, which would indicate, again, embolic phenomenon, as well as, of course, as I said, [auscultated] the heart.”

After his examination of Kurt, Dr Dobler recalls contacting the infectious diseases department at John Hunter Hospital for advice in relation to Kurt’s positive blood culture. According to Dr Dobler, “The advice was that this type of germ would be very unlikely to be a pathogenic bacteria in a patient who was not severely immuno-compromised or did not have an artificial valve in place, and their advice was that if there were no signs of endocarditis then it would be prudent to repeat the blood culture after a short course of antibiotic, but they felt reassured by the nature of the bacteria and the other illness that was going on and the white cell – the neutrophil count being relatively normal.”

Mr Halverson saw Kurt both before and after going to work that day. When he returned to the hospital after work Kurt was suffering from a pain in the abdomen. Mr Halverson had brought Kurt some magazines and had started to read them out to him. Kurt was in a lot of pain and, with his back to his father, asked if he would “please shut up for a while.” Mr Halverson had now become very concerned about Kurt’s health and was troubled by the report of a heart murmur. He asked Kurt if Dr Dobler had sounded his heart again and whether it was OK. Mr Halverson remembers that Kurt replied in the affirmative, although he could not recall his exact words. Records show that Dr Dobler saw Kurt again that night.

Dr Dobler’s notes for the next day (9 February 2001) state: “Much improved. Reduce intravenous fluids. Cervical nodes ? discharge this evening.” Dr Dobler was questioned about this note: “Q. Can you interpret that for us? A. Again, my recollection is that on that day I did again do a physical examination involving an examination of the heart and abdomen, the only positive finding being that of swollen cervical lymph nodes and a general observation that the patient was significantly better. Q. And the examination of the heart that you’ve referred to, what did that involve? A. [Auscultation] of the anterior chest wall. Q. Do you have a recollection? A. Yes, I do. Q. And what was your recollection as to the result of that? A. I recall that I could no longer hear a murmur.”

That night Dr Dobler saw Kurt again when he was doing unscheduled rounds of the Hospital. His notes record that Kurt had had a dystonic reaction to Stemetil/Promethazine. Dr Dobler described a dystonic reaction as “a reaction that occurs to certain medications which can impact on the ability to control the muscles of the face and the eyes, and so a common presentation would be that the eyes are deviated to one side or that the head is deviated to one side or that the tongue is deviated to one side. This is a severe sort of spastic-type reaction in terms of the muscle goes into quite significant spasm – quite frightening for the person who is undergoing it and certainly for those able to observe it.” Dr Dobler recalls that by about 7:30 this reaction had “resolved” after Kurt was given Cogentin. Kurt remained in hospital that night.

Dr Dobler saw Kurt again the next morning (10 February 2001). Mr Halverson was present. Kurt appeared much better and he very much wanted to go home. Dr Dobler’s notes state: “Doing well. Still febrile. May go home. Continue conservative management. Repeat bloods on Monday.” There is no record of a physical examination.

Dr Dobler said that he recalls that he performed an examination on Kurt that morning, although he did not record it. He gave the following evidence: “Q. Do you have a recollection in relation to that occasion, independent of the note? A. Yes. I recall that I again performed an examination upon Kurt, including [auscultation] of the heart, palpation of the abdomen, as well as having access to the observations. Q. All right. When you say “[auscultation] of the heart,” is that, as we’ve been over, the stethoscope? A. And could not detect a murmur.”

In a letter which he wrote on 11 February 2001 after Kurt had suffered his cardiac arrest, Dr Dobler wrote “On 10/2 he had a low grade fever but felt well (the murmur was not now audible).” In the same letter he described the murmur that he had originally detected as being 1/6, when in his earlier records it is shown as 2/6.

Mr Halverson’s evidence with respect to Dr Dobler’s examination of Kurt on 10 February was as follows: “Q. While you were present on that morning, that is 10 February, and during Dr Dobler’s visit, did you observe any examination of Kurt by Dr Dobler? A. No. Q. Have you seen a doctor using a stethoscope? A. Yes. Q. Did Dr Dobler examine Kurt in your presence with a stethoscope? A. No, he didn’t.”

I am satisfied that Mr Halverson gave an accurate account of what he saw. This does not preclude Dr Dobler from having examined Kurt when his father was not present although the fact that there is no record suggests that Dr Dobler’s recollection may be faulty.

As it happens I do not believe it is necessary to resolve this conflict between the recollection of Mr Halverson and Dr Dobler. However, if it had been necessary I would have preferred the evidence of Mr Halverson. At this point the progress of Kurt was not unusual and there would be little, without a note, to mark these events in Dr Dobler’s memory. Mr Halverson’s situation was quite different. His heightened concerns would have made it likely that events would be remembered with clarity and in detail. The night of 10 February and the morning of 11 February 2001 – Kurt has a cardiac arrest

When Kurt arrived home his parents were sufficiently concerned that they tried not to leave him on his own at any point. Mr Halverson required Kurt to shower in the ensuite to the master bedroom so that if anything went wrong Mr Halverson (who was sitting on the bed within earshot) could respond promptly. Kurt’s sister Annika’s room was situated next to Kurt’s. That night Mr Halverson changed beds with her so that he could be near Kurt in the event of anything happening. As it happens this was a prudent step although ultimately he could not prevent the catastrophe which was to occur in the early hours of the morning of 11 February. Mr Halverson described the sequence of events in the following terms: “Q. Did you all retire at about 10 o’clock? A. Thereabouts. Q. In the early hours of the morning, were you awoken by something? A. Yes. Q. What was it? A. I think it was a noise, but something woke me. Q. What did you do? A. It woke me to the point where I jumped out of bed and I went into the little hallway between the room that I was sleeping in and Kurt’s room to look at him. Q. And, yes? A. Because the lights were all out, but I could see a silhouette of Kurt and from what I could see in the dark, it appeared that he was partially raised up on one arm and he was making some very strange noises. My best description of those would be long exhalations. Q. Exhalations? A. Yes, it was as if he was breathing out but restricted and prolonged. I turned the light on and called for Jan. Q. In what manner did you call for her? A. From the way she responded I would say it was fairly loud. Q. What did you see when the light went on? What did you see of Kurt? A. Kurt was on his back. He had gone on his back and he was a very unusual colour, he was very pale but an unusual colour. Q. Were his eyes open or closed? A. His eyes were closed. Q. And then what happened? A. Jan had come in and immediately felt for a pulse and she said there was no pulse and the noises that Kurt was making had ceased, and Jan told me we had to do CPR very quickly, had to start, and I tried to commence CPR. There seemed to be a lot of mucus around Kurt’s face and I tried to do CPR but his cheeks were filling up, but his chest wasn’t – his cheeks were blowing up but his chest wasn’t and I wasn’t doing any good and I realised that I was being fairly silly doing it on a soft bed as well, so I picked Kurt up and put him on the floor and realised that if I didn’t – I realised that if I didn’t get some air into him, he would die. I couldn’t feel anything obstructing his – so I blew as hard as I could and whatever was obstructing cleared and I started to get air into his lungs, and Jan and I were doing CPR together and one of us left to ring Ken Dobler – I can’t remember who. I remember speaking to Jill – Q. Just pause there, if you would, Mr Halverson. While you were trying to clear the blockage, do you recall seeing anyone else present? A. Yes. Q. Who? A. Annika came into the room. … Q. What was Annika doing? A. She was just standing there. Sorry, I didn’t want her to see her brother die, so I contacted my sister [Jill] to come and get her. … Q. All right. An ambulance arrived? A. Yes. Q. And Dr Dobler arrived, right? A. Ken arrived not long after the ambulance, a few minutes, although he had come all the way from Broke. … Q. When the ambulance officers arrived, did they take over straightaway and continue the attempts to resuscitate Kurt? A. Yes. Yes. They asked me to stop as soon as they came in and they took over. … Q. You told us that Dr Dobler had come all the way from Broke. That’s about what distance? A. From where Ken lived to our place would be a little bit over 30 kilometres. Q. A bit over 30. Did you notice him when he arrived? A. Yes, I was outside when he arrived, when he got out of his car. Q. Did you notice anything about him? A. Yes. He appeared quite upset and his eyes were very damp. Q. He immediately went to see Kurt, who was being loaded into the ambulance; is that right? A. Yes. He checked to see what the paramedics were doing and pretty well took over and got in the ambulance with Kurt. Q. As Kurt was being loaded into the ambulance, did you notice something about his arm? A. Yes, one of his arms flopped off the narrow stretcher and struck some heavy steelwork at the back of the ambulance, and it just flopped, it was just like a corpse. He was just totally flaccid and still.”

The ambulance took Kurt to Cessnock Hospital and from there he was flown by helicopter to John Hunter Hospital. Notwithstanding the care he received the cardiac arrest had already done irreparable damage to his brain.

Mr Halverson gave evidence that a few days later Dr Dobler explained to the Halversons that he believed that Kurt’s viral illness had had an impact on his heart which caused a heart attack. He told them that Kurt’s prognosis was not good but that he might be able to recover to some extent. He said that the Halversons were lucky that Kurt had suffered the attack at home because if it had occurred in hospital it would not have been noticed and Kurt would have died. Dr Dobler’s evidence with respect to an ECG and other matters

Dr Dobler gave evidence that ECG facilities were in use at Cessnock Hospital in 2001. A self interpreting machine was available which automatically measured the patient’s QT interval. Dr Dobler was asked why he did not, at any stage, order an ECG. The following exchange occurred: “Q. From that method of ongoing education and your general learning, by 2001 what do you say were your primary reasons for not ordering an ECG? A. My understanding at that period of time was that an ECG wasn’t indicated, in that there were no symptoms which directed me towards the heart as a cause of the syncopal episodes, and my understanding was that determining the cause was based on history and examination and then being directed by abnormal findings in that regard, such that, in all of Kurt’s cases that had been described for Kurt, these events were, to me, quite explicable on a non-cardiac basis. Q. Let’s just assume that, contrary to your recollection, you were aware of this alleged episode of 29 June 1998 about the temporary loss of consciousness whilst coming to your surgery. Would that have changed your view? A. No, I don’t believe so. Again, this reflected, to me, from the description, a quite classical fainting episode with him being dizzy from the time of getting out of the car, to requiring assistance to move down the pathway, having a premonitory sign of knowing that he was going to faint or he was going to pass out and having a postural element, such that he was standing at the time, and also it was clearly in the presence of an intercurrent illness. Q. In the event of some of these episodes not being associated with a viral illness, would that impact upon the clinical presentation? A. Well, a viral illness may only be one triggering factor. If there was no suggestion of any intercurrent illness or event, such as extreme pain, emotional disturbance, then it may change my view that, yes, a cardiac cause needed exclusion. Q. What if there were no premonitory signs? A. Again, that would be more suggestive of a cardiac or neurological cause for syncope. Q. In those events, would you do an ECG? A. In all likelihood.”

Dr Dobler accepted as a fundamental principle of diagnosis that where a patient presents with symptoms that are susceptible to more than one diagnosis, any diagnosis with lethal potential or a serious morbidity risk should be established and treated or an attempt made to rule it out by establishing a valid alternative diagnosis. He also accepted that a cardiogenically determined syncope has a lethal and/or serious morbidity potential.

Much of the cross-examination of Dr Dobler was concerned with whether he accepted propositions from a well known text – Murtagh’s General Practice . Dr Dobler accepted that Murtagh was respected by Australian GP’s and commonly used by them. Dr Dobler accepted that the key to an accurate diagnosis in the context of syncopal episodes is the taking of a very careful history. The patient must be taken second by second through the incident and as many eyewitnesses as possible must be spoken to. He also accepted that the details of the history should be carefully and thoroughly recorded, especially when the syncopal event is undiagnosed. Dr Dobler agreed that the history he had recorded in relation to Kurt’s faint of 4 September 1995 was nothing like the sort of detailed history envisaged by Murtagh. He accepted that if he had been given an oral history of the events of 29 June 1998 consistent with Mr Ron Halverson’s (i.e. Kurt’s grandfather’s) evidence then his notes in relation to that incident would represent a “gross breach” of the principles in Murtagh. However, he did not accept that even with knowledge of the 1998 collapse cardiological investigations would have been appropriate.

Dr Dobler was questioned about the effectiveness of his diagnosis and the response to Kurt’s symptoms which he would make today: “Q. Doctor, will you accept from me that these last questions are not put in any gratuitously accusatory manner when I ask you this: in retrospect, it’s clear that Kurt fell through the diagnostic cracks, did he not? A. I think, in retrospect, the diagnoses which I made were consistent with his presentation. However, I would agree, in retrospect, that he has suffered an event for which I’ve not considered the possibility. Q. And beneath those diagnostic cracks there was, we know, the potential for a catastrophic outcome? A. We know that in retrospect, yes. Q. Recalling your agreement at the beginning of this cross-examination with the basic principle of diagnosis we discussed and your acceptance of Murtagh’s principles of garnering and recording histories, has this tragedy led you to a more careful observation of those tenets I have just referred to? A. I believe that it has. Q. Doctor, retrospective wisdom we know is easy, but those truths that I have just referred to existed in 1995, 1998, 2001, just as they do today, did they not? A. That’s correct. Q. And, indeed, throughout that whole period, they were there to be observed, were they not? A. Yes, they were.” The evidence of five general practitioners

The plaintiff called two expert general practitioners, Drs Chambers and Mackey. The defendant called three expert general practitioners, Drs Bunker, Ford and Walsh. They are all highly qualified and experienced.

Dr Chambers received her MB BS (Hons) from UNSW in 1975. She has been a full time GP in Sydney since 1988 and a Fellow of the Royal Australian College of General Practitioners (FRACGP) since 1993. She has been an examiner for the RACGP since 1994 and a Clinical Supervisor for the RACGP training program since 1995. She is a Clinical Lecturer in the Department of General Practice at the University of Sydney.

Dr Mackey also received his MB BS from UNSW in 1975. He joined the medical practice at Scone in 1977 before moving to the single-doctor town of Lockhart in 1989. He is a Visiting Medical Officer at a small rural hospital. Amongst other things, Dr Mackey is a Fellow of the Australian College of Rural and Remote Medicine (FACRRM), a member of the NSW Rural Doctors Association Management Committee (he was President from 1999 to 2001) and he was President of the Rural Doctors Association of Australia between 2001 and 2003.

Dr Bunker received his MB BS (Hons) from UNSW in 1983 and was awarded, inter alia, the University Medal. He became a FRACGP in 1994 and has been a supervisor for the RACGP Training Program since 1992. He worked as a GP in Ultimo between 1986 and 2004. Since 2003 he has been the Director of Training at the Sydney Institute of General Practice Education and Training and he has been a Staff Specialist at the Fairfield Hospital GP Unit since 2004.

Dr Ford received his MB BS from the University of Melbourne in 1978. He has been a GP and VMO in the rural Victorian town of Hamilton since 1985. He became a FRACGP in 1985 and an FACRRM in 2000. Amongst other things, Dr Ford is an Honorary Senior Lecturer in the School of Medicine at Flinders University.

Dr Walsh received his MB BS from the University of Sydney in 1981. From 1983 to 1989 Dr Walsh worked in medicine in a variety of rural areas including Scone, Coonabarabran, Bowen and Meekatharra. From 1989 he has worked as a GP in Annandale. He became an FRACGP in 1988. He has been Chairman of the Dermatology Update for General Practitioners Postgraduate Committee in Medicine of the University of Sydney since 1994.

There were significant differences between the responses of the general practitioners to some critical questions. As with the cardiologists, the general practitioners gave evidence concurrently having first identified the issues on which they agreed and those on which they disagreed. Although all of the doctors brought a useful perspective to the various problems to my mind Dr Mackey’s evidence was of the greatest assistance. He presently practices in a small country centre at Lockhart and has practiced in rural areas for thirty years. I am satisfied that his view of the appropriate responses to be expected of Dr Dobler were entirely reasonable.

I was also impressed by Dr Bunker, who was prepared to make reasonable and appropriate concessions which tended to qualify his primary position. This was not always the case with Drs Ford and Walsh. The position is clearly demonstrated by the evidence they gave as to whether the clinical note made by Dr Dobler on 29 June 1998 of the single word “migraine” was adequate. Drs Ford and Walsh said that it was, but Dr Bunker conceded that a more detailed note was required. I have no doubt that the note which Dr Dobler made was insufficient.

Dr Chambers impressed me as a careful and competent general practitioner. Because her practice is city based, with access to teaching hospitals and other high level facilities, I do not rely primarily on her views when they differ from the other doctors, particularly Dr Mackey. Dr Dobler’s professional conduct must be assessed having regard to his training and experience and the facilities available to him at Cessnock.

All of the general practitioners agreed that it was appropriate and sufficient for Dr Dobler to have ordered an EEG and referred Kurt to a neurologist following the syncopal event in 1995. None of the doctors believed that Dr Dobler should have instituted a cardiac investigation once the EEG was established to be normal. However, both Drs Chambers and Mackey emphasised that the test results would remain on the record and should have continued to be a valuable diagnostic aid. This must be so.

Drs Mackey, Ford, Walsh and Bunker agreed that at the time of the EEG an appropriate provisional diagnosis of the 1995 event was of vasovagal faint. Although Dr Chambers was of the view that, particularly because Kurt fell into his food, the event was probably not vasovagal she agreed that at the time it was reasonable for Dr Dobler to have made a provisional diagnosis to that effect.

As I have related, Kurt later underwent a second EEG following sleep deprivation. Again, no neurological irregularity was indicated. Although it was agreed by all of the general practitioners that such a result would not have suggested a cardiological disorder, Dr Mackey and Dr Chambers noted that the results increased the probability of a non-neurological cause, including a cardiogenic cause. Because there are only three major causes of syncope, vasovagal/hypotension, neurological and cardiological, the position taken by those doctors is logical. As the possibility of a neurological cause recedes the other two must both require greater consideration. However, Drs Bunker, Walsh and Ford thought that an increased probability of a non-neurological cause made a provisional diagnosis of vasovagal syncope more likely. The three of them indicated that a cardiological cause would still not have entered their thinking at this point. I did not find that conclusion convincing and to my mind good medical practice should have kept the possibility of a cardiological cause in mind until eliminated.

In relation to the 1998 event, all of the doctors were of the view that Dr Dobler should have “elicited and recorded a detailed history” of the event. However, when the doctors were asked whether, “in the circumstances of Kurt’s attendance at the defendant’s surgery on 29 June 1998, did the defendant exercise the standard of care required of him by simply diagnosing and recording simply “migraine,’” only Drs Mackey, Chambers and Bunker answered “no.” To my mind, the single word “migraine” could never constitute a “detailed history” commensurate with a GP’s standard of care.

Upon the assumption that Kurt had lost consciousness outside Dr Dobler’s surgery in 1998, and that Dr Dobler had been informed of this, Dr Chambers and Dr Mackey were of the view that further investigations were warranted at this point. In the context of Kurt’s repeated headaches and other symptoms, and in light of the syncopal event of 1995, they believe a CT scan of the brain was called for. Dr Mackey (with whom Dr Chambers agreed) said that once this neurological avenue had been exhausted, “the other critical limb of diagnosis should be a cardiological cause, and I would be progressing along that pathway at this stage, I think, or near to this stage. One of the easiest and simplest diagnostic procedures I would undertake would be an ECG.” Drs Walsh, Ford and Bunker were all of the view that the 1998 syncope, as well as Kurt’s other symptoms (ie the light headedness, déjà vu, headaches and other symptoms that had persisted for some time prior to the 1998 event), did not suggest a cardiological cause and could be otherwise explained. To them, Kurt’s symptoms were consistent with the diagnosis of migraine and the syncopal episode was typical of a vasovagal faint.

There was also disagreement between the general practitioners as to the approach which should have been taken to the events which occurred in February 2001. The series of events of acute illness, the detection of a heart murmur followed by a collapse, and the diagnosis of glandular fever must be considered having regard also to the knowledge of previous events which was available to Dr Dobler.

Although the matter has not been easy to resolve, I have come to the conclusion that the opinion of Dr Mackey, and in so far as she agrees with Dr Mackey, the view of Dr Chambers, should be accepted in relation to the response which Dr Dobler should have made to the February events. The starting point for the analysis is that Dr Dobler reported a 2/6 pansystolic murmur on 1 February. Whether he was competent to do so or whether he misreported his findings is of no relevance. He was required to respond to the symptoms he had found and reported. For this reason the initial views of Drs Walsh, Ford and Bunker are not of particular assistance. They doubted whether a general practitioner could confidently identify a murmur as pansystolic. For that reason their initial position was that no cardiac investigation was required.

Their positions were modified when they were asked at least to accept that Dr Dobler believed he had identified a pansystolic murmur. All of the doctors agreed that in these circumstances an x-ray was not appropriate. Dr Walsh acknowledged that an echocardiogram should have been done, as did Drs Bunker, Ford, Mackey and Chambers. Dr Chambers and Dr Mackey were of the view that an ECG should also have been done.

The divergence of opinion between the general practitioners when considering the response which should have been made by Dr Dobler to the syncopal event on 4 February 2001 is of critical significance to the resolution of this case.

Dr Chambers stated her position emphatically: “We have had a history building up over time. We know that there is the possibility of these problems that are associated with syncopal attacks. The man is in hospital and we have had a cumulative history of funny turns that are not really properly explained. We have negative neurological investigations, we have a further funny turn, be it seizure, be it faint, be it drop attack – whatever it is. The man is in hospital, he has easy access to do all of the appropriate investigations.”

When giving evidence Dr Chambers later elaborated further: “He has ample opportunity and has used the advantage of a neurological opinion. He had also opportunity, easy opportunity whilst he was in hospital to begin some cardiological investigation that was there on tap in Cessnock Hospital with an ECG and a monitor.”

Dr Mackey said that even if the heart murmur had not been detected, an ECG would have been warranted after the syncopal event on 4 February 2001. Both of the plaintiff’s doctors had said something similar in their earlier individual reports. In her report of 16 February 2006, Dr Chambers stated that Kurt’s presentation on 4 February 2001 was unusual and not typical of a vasovagal syncope. Since Kurt was in hospital at the time, “access to investigation and specialist review was more easily available.” She believed that a reasonable GP would have organised: routine blood tests, ECG, cardiac echo, sleep deprived EEG, review with a cardiologist (for Holter monitoring, electrophysiological studies and a tilt-table test) and review with a neurologist. In his report of 14 March 2006, Dr Mackey pointed out that Kurt was admitted as a result of glandular fever which was unusual for someone of his age unless the condition was severe. His test results in relation to the glandular fever would be considered mild to moderate. However, his presentation with a syncopal episode should have resulted in further investigation. “Whilst in hospital there is easy access to ongoing observation and an ECG would have been relevant and easily accessible. I consider this the first and basic [sic] investigation at this stage of the illness.”

The other doctors were of the view that all of Kurt’s syncopal events, as well as his other symptoms, were explicable in terms of vasovagal faints, intercurrent illness and migraines, and that on this basis there was no cause for pursing cardiological investigations following the 4 February syncope. In his report of 5 July 2006, Dr Walsh stated: “There was no indication for Dr Dobler to perform an ECG as the circumstances of the plaintiff’s syncopal episode on 4 February 2001 were broadly similar to previously investigated episodes. In addition, he was suffering from an acute viral illness which would be likely to reduce blood pressure and aggravate any predisposition to vasovagal syncope. There was nothing to alert Dr Dobler to the possibility of cardiac syncope at any point in the plaintiff’s course, in my opinion. In my experience, general practitioners do not perform ECGs or blood tests routinely on teenagers suffering apparent vasovagal syncope, particularly if they have been assessed by a specialist in the past.”

Dr Ford expressed a similar view in his report of 25 July 2006.

Dr Bunker took a slightly different tack in his report of 7 August 2006. He noted that when Kurt was admitted to Cessnock Hospital following the syncopal episode of 4 February 2001, Dr Wakatama recorded a loss of consciousness following a change in posture with prodromal symptoms of dizziness. Dr Wakatama did not order an ECG. Dr Dobler reviewed Kurt the next day. Dr Bunker said “I believe many of my peers would not have performed an ECG in this clinical setting.”

It was accepted by all the GPs that if an ECG and echocardiogram had been performed after 4 February 2001 and had yielded normal results, they would have concluded that Kurt’s heart was normal.

The divergence of opinion about whether Dr Dobler should have obtained an ECG may be due to the fact that some of the opinions, notably those of Dr Walsh and Dr Ford, expressed a view as to the response of a general practitioner when seeing a patient in his or her practice, whereas Dr Mackey and Dr Chambers emphasised that at this point Kurt had returned to hospital. Although an echocardiogram was not available at that hospital an ECG was and the test could have been readily initiated. The fact that Dr Wakatama did not ask for an ECG is not of moment – she did not know of Kurt’s previous history of collapse. But, of course, Dr Dobler did and he also knew that two neurological investigations had returned negative results. With the repetition of syncopal events Kurt either had repeated benign events or had a cardiac problem. Although Dr Bunker said that many of his peers would not have performed an ECG in this clinical setting the diagnostic material available to Dr Dobler was not confined to the events on or near to 4 February 2001. To my mind Dr Dobler should have requested an ECG. Kurt was in hospital and the ECG facility was immediately available and takes very little time to arrange.

Professor Saul, who is a specialist cardiologist, also expressed an opinion about this aspect of the matter. Like the other cardiologists who gave evidence his opinion as to the appropriate response of a general practitioner is relevant. In his opinion it was almost beyond comprehension that at the point of the 4 February event Dr Dobler did not ask for an ECG and refer Kurt to a cardiologist. Both Professor Harris and Associate Professor McGuire, speaking of course as cardiologists, would have ordered an ECG following the 4 February episode. Associate Professor Richards was also of the view that an ECG should have been carried out. The Evidence of Dr Silberberg, Cardiologist

The defendant called Dr Silberberg who is a cardiologist. He is the cardiologist to whom Dr Dobler commonly referred patients. He was called to give evidence of the likely course of events if Dr Dobler had asked for his advice or referred Kurt to him. Dr Silverberg has 20 years experience as a cardiologist and has been practicing in the Newcastle area since 1989. Prior to 2001, Dr Silberberg had treated hundreds of patients who had presented with syncope.

Dr Silberberg’s opinion was that Kurt’s syncopes were probably vasovagal and were precipitated by an intercurrent viral illness. He noted that “an intercurrent illness will precipitate all sorts of reactions, like faints, and even seizures, in someone who is predisposed.” If consulted in February 2001 he said he would have recommended a neurological re-evaluation of Kurt, but believed there was nothing to indicate that Kurt’s symptoms had a cardiological cause. He was not troubled by Kurt’s heart murmur, which he believed could also have been caused by his viral illness. If he had been contacted by Dr Dobler, his advice would have been to wait for the illness to pass and then check to see if the murmur was still present. Only then would further action be taken.

Significantly, Dr Silberberg said that if Kurt had been referred to him he would have obtained an ECG. The following evidence was elicited in cross-examination: “Q. If you were asked to have a look at [Kurt], an ECG would be one of the first things you would have done? A. Yes, sure. … Q. Whatever the family history, you would certainly, as a cardiologist, [if a patient was referred to you after three undiagnosed syncopal events], have instituted an ECG, wouldn’t you? A. Yes, I would have done an ECG. … Q. Doctor, whatever be the symptoms at that point [i.e. following a third syncopal event], you would have accepted him as a patient, would you not? A. Always. If a patient needs to see me, in anybody’s perception, be it the patient’s or the doctor’s, I’ll see them. … Q. Once again, doctor, if you had been asked to review him, you would have, by your lights, done a thorough cardiological investigation of this lad? A. Sure. Q. Bearing in mind the lethal potential bespoken by a cardiogenic cause of these syncopal events; correct? A. I would have been very thorough.” The evidence of Dr Raftos

Dr Raftos was called by the plaintiff to give evidence in relation to the appropriate response of medical staff at a hospital when faced with problems of the type experienced by Kurt. Dr Raftos graduated with honours from the University of Sydney in 1976 and has been a registered medical practitioner since that time. He has been a Specialist in Emergency Medicine since 1983, in which year he also became a Fellow of the Australasian College for Emergency Medicine. He has been Director of Emergency Medicine at Sutherland Hospital since 1984, a Senior Specialist in Emergency Medicine at St Vincent’s since 1997 and a Senior Specialist in Emergency Medicine at Sydney Hospital since 2004. He has been a conjoint lecturer at UNSW since 1990.

In relation to his knowledge of what will provoke a long QT interval, Dr Raftos was of the view that on the basis of his experience he knew as much about the subject as any cardiologist except a cardiologist who had a special interest in the subject. He conceded that predictions about whether an ECG would reveal a long QT interval at any given time were more within the domain of such cardiologists than within his own.

In his report of 24 March 2006, Dr Raftos reviewed Kurt’s medical history and said “it is clear in retrospect that Kurt’s illness that began in about September 1995 and was characterised by several collapses unconscious, along with headaches, lightheadedness, feelings of déjà vu, altered sensation and muscle power, was due to recurrent episodes of ventricular tachycardia caused by congenital long QT syndrome. The description of his “migraines” [as recorded by Dr Dobler] is a typical description of the effects of short, self-limited runs of ventricular tachycardia.” In the same report, Dr Raftos states that all patients who present to a hospital emergency department with syncope should be given an ECG. In relation to the period from 1 to 11 February 2001, Dr Raftos said: “Kurt became unwell in late January 2001 and went to see Dr Dobler on 1 February 2001 because of extreme fatigue. During the examination Dr Dobler found a heart murmur ("2/6 pansystolic murmur radiating to axilla") that had not been present previously. He responded to the murmur by ordering a chest xray that was performed on 2 February 2001 and reported as normal. The appropriate response to the presence of a new heart murmur is to perform electrocardiogram and chest xray and to arrange consultation with a specialist cardiologist. The appointment with the cardiologist can safely be at a convenient time for a patient who is otherwise well. However, Kurt's murmur was discovered at a presentation for extreme fatigue and so the need for consultation was urgent. He should have seen a cardiologist within days of the discovery of the murmur. The cardiologist would, among other things, have performed an echocardiogram which would, on the balance of probabilities, have been abnormal. Dr Dobler's failures to perform an electrocardiogram and to refer Kurt urgently to a cardiologist in response to the discovery of a new heart murmur represent significant departures from the accepted standard of medical care at the time. Electrocardiogram would, on the balance of probabilities, have shown diagnostic evidence of long QT syndrome. Echocardiogram would, on the balance of probabilities, have shown evidence of mitral valve regurgitation and left ventricular hypertrophy/strain. Had these investigations been performed, their results would have led to Kurt being admitted to a cardiology facility where the causes of his cardiac abnormalities would have been further investigated and treated. He would, on the balance of probabilities, not have developed ventricular fibrillation on 11 February 2001 and its attendant brain injury. Kurt had a further episode of unconsciousness on 4 February 2001: "stiffening of limbs & ? loss of colour for - 20 secs at home" and was taken to Cessnock Hospital. The doctor [Dr Wakatama] noted: "Tonight got up to get a drink of milk & felt dizzy & ? fainted. Father caught him & he had some stiffening of limbs & then went limp LOC 30 secs." This was clearly an episode of syncope, collapse unconscious, and an electrocardiogram was an essential part of appropriate investigation, given that cardiac arrhythmia is an important cause of syncope… Electrocardiogram performed on 4 February 2001 would, on the balance of probabilities, have shown QT interval prolongation and this would have led to a diagnosis of long QT syndrome. Appropriate treatment would then have significantly reduced the likelihood of ventricular fibrillation. Dr Dobler saw Kurt on 5 February 2001. Dr Dobler had personally diagnosed a new murmur on 1 February 2001 and now became aware that Kurt had had another episode of collapse unconscious. The combination of these two events strongly suggested that a cardiac abnormality had caused Kurt's syncope. It would be reasonable to expect that an ordinary skilled doctor would have performed an electrocardiogram and referred Kurt urgently to a cardiologist at this stage. The failure to perform an electrocardiogram and to obtain an urgent cardiologist consultation in these circumstances represents a significant departure from the accepted standard of medical care at the time. Electrocardiogram performed on 5 February 2001 would, on the balance of probabilities, have shown QT interval prolongation and this would have led to a diagnosis of long QT syndrome. Appropriate treatment would then have significantly reduced the likelihood of ventricular fibrillation.”

In the re-examination of Dr Raftos, the following exchange occurred: “Q. Just one other thing: you were asked about what you felt should be practice in the context of recurrent syncopal episodes in a male teenager. Do you perceive any logical distinction between an urban and a country approach by a general practitioner in that context? A. No, this isn’t complex specialist or sub-specialist medicine. This is very simple medicine. The patient presents with a syncopal episode, simple tests to exclude cardiac disease, including electrocardiogram. It’s not complex medicine, it’s very common medicine that primary care people, GPs and emergency departments, practice every day or every week and it doesn’t require any specific technology or any specific specialist knowledge”

I accept Dr Raftos. His evidence reinforces the view that Dr Dobler should have obtained an ECG following Kurt’s collapse in February. By failing to obtain an ECG Dr Dobler breached the duty of care which he owed to Kurt. The nature of the syncopal events and appropriate response – four eminent cardiologists

Four cardiologists, each highly qualified and experienced gave evidence.

The plaintiff called Professor Saul and Associate Professor Richards. Professor Saul is a Paediatric Cardiologist who resides and works in South Carolina in the USA. Professor Saul received his BS from Duke University in 1978, graduating magna cum laude. He received his MD from the Duke University Medical School in 1982. He has lectured and held positions as Assistant Professor, Adjunct Professor and Associate Professor at Harvard Medical School and the Harvard-MIT Division of Health Sciences and Technology, and he has published some 152 articles and 28 book chapters. He has been a Professor of Pediatrics, Cell Biology and Anatomy at the Medical University of South Carolina (MUSC) since 1997, and he is presently the Chief of Paediatric Cardiology and Medical Director at the MUSC Children’s Hospital. He has been the Director of the Children’s Heart Program of South Carolina since 1997, and was the Director of the Cardiac Arrhythmia Service at the Children’s Hospital in Boston between 1997 and 2001. He holds and has held a wide variety of memberships, appointments, awards and positions of significance in his distinguished professional career.

Associate Professor Richards received his MD from the University of Sydney in 1984, and has been a Clinical Associate Professor at that university since 1999. He is a Fellow of the Royal Australian College of Physicians (FRACP) and the American College of Cardiology (FACC). He was a Senior Staff Specialist at Westmead Hospital between 1984 and 1993, and in the past has been a Consultant Cardiologist at Hills Private Hospital and Sydney Adventist Hospital. He is presently a Visiting Cardiologist at Westmead Hospital and Westmead Private Hospital, and a Consultant Cardiologist at New Children’s Hospital and Mater Misericordiae Hospital. He is a reviewer for numerous respected journals such as the Medical Journal of Australia , the Journal of the American College of Cardiology and the British Heart Journal. He is also an examiner for the Royal Australian College of Physicians and the Australia and New Zealand College of Anaesthetists.

The defendant called Professor Phillip Harris and Associate Professor Mark McGuire. Professor Harris has been the Head of the Department of Cardiology at Royal Prince Alfred Hospital since 1985, a Senior Staff Specialist since 1986, and a Clinical Professor at the University of Sydney since 1992. He was awarded a D Phil from Oxford University in 1970. He is a FRACP and a FACC, a Fellow of the American Heart Association (FAHA) and a Fellow and Life Member of the Cardiac Society of Australia and New Zealand (FCSANZ). Professor Harris was the President of the last mentioned Society between 1996 and 1998. He holds and has held a number of other appointments, memberships and positions of significance, including President of the NSW Division of the National Heart Foundation from 1996 to 2003. Professor Harris is currently a member of the National Heart Foundation Board of Directors) and Chair of the Patient Care Committee at Royal Prince Alfred Hospital.

Associate Professor McGuire is a Senior Staff Specialist and Director of the Cardiac Arrhythmia Service in the Department of Cardiology at Royal Prince Alfred Hospital, and a Clinical Associate Professor at the University of Sydney. He received his PhD from Sydney University in 1993, and his undergraduate career is marked by distinction. He is a FRACP and a FCANZ, and a Member of the North American Society of Pacing and Electrophysiology. He is a member of the Editorial Boards of the Journal of Cardiovascular Electrophysiology and Heart Rhythm , and is or has been a reviewer for several respected journals. He has published an extensive body of work, and has been an invited lecturer at numerous national and international conferences.

Each cardiologist prepared at least one written report and they met prior to giving their evidence in order to refine the issues falling within their areas of experience. They gave evidence concurrently, Professor Saul participating by way of video link. This process proved both highly productive and efficient and has been of great benefit to me in resolving this case. The discussion was sustained at a high level of objectivity by all participants, each of whom displayed a genuine endeavour to assist the court to resolve the problems. The fact that ultimately they disagreed on critical issues was not due to anything other than a genuine difference of opinion about the appropriate conclusion to be drawn from the known facts.

Given my finding that an ECG should have been performed, the next question is whether or not it would have revealed an abnormality. This is the ultimate question addressed by the cardiologists who commenced by reviewing Kurt’s medical history. The 1995 episode

In relation to the syncopal episode on 4 September 1995, Associate Professor Richards and Professor Saul believe the cause was most likely a cardiac arrhythmia, whereas Professor Harris and Associate Professor McGuire believe the cause was more likely to be vasovagal or hypotensive.

In his earlier reports, Associate Professor Richards had come to a different conclusion. He had initially thought that the 1995 syncope was vasovagal. In relation to his subsequent change of opinion, the following evidence was elicited: “MR HIGGS: Based on that history [i.e. the history contained in Dr Wilkinson’s letter], do I take it that in your opinion the events described there are classically vasovagal, consistent with the opinions that you expressed in your report of 10 May 2003? PROF RICHARDS: This description is obviously different from subsequent descriptions of the event, and based on this description and the conclusion of Dr Wilkinson was the reason that at the time my initial report was written, without the subsequent knowledge, I thought that this sounded vasovagal. MR HIGGS: Right. What is the additional information that you say causes you to change your opinion? PROF RICHARDS: In the letter that you have shown me here it says that the food tasted unpleasant. At that stage, he looked very pale and his head slumped forward and he fell out of his chair. The description from my recollection of the evidence here in court was that he fell head first into his plate. MR HIGGS: The fact of the food tasting unpleasant, would that classify as a prodromal event, in your view? PROF RICHARDS: No. Bad cooking. MR HIGGS: Do you seriously suggest that? PROF RICHARDS: It doesn’t sound like a prodrome. Poor taste of food is not a prodrome that I’m aware of. … MR HIGGS: You are saying that the food tasting unpleasant was irrelevant to [your initial conclusion that the event was vasovagal]; is that right? PROF RICHARDS: Given that he was unwell during the day, that was a more likely cause for his food tasting different to him. MR HIGGS: Is the only difference in the history the fact that he fell forward into his food rather than him having his head slumped forward and his [sic] fell out of his chair? It’s the direction in which he fell. That’s the difference is it? PROF RICHARDS: Yes. MR HIGGS: Why is it that and that alone alters your view? … PROF RICHARDS: In the circumstances of a faint, the patient will usually feel unwell and generally then slump to the floor. From the description here [i.e. in Dr Wilkinson’s letter] it sounds to me as if the food tasted bad and he slumped to the floor. In the subsequent description, I am not sure that the food taste was reported, but it is described that without warning he fell forward into his food, and that’s the difference to me.”

In light of this evidence, I reject the suggestion by the defendant that the reason for Associate Professor Richards’ change of opinion was the fact of Kurt’s cardiac arrest. It is clear that the real reason is that, having regard to subsequent descriptions of the event, Associate Professor Richards came to the view that the collapse was more sudden than the description in Dr Wilkinson’s letter would suggest. In this regard, he said: “I think that all of us have understood the facts better as the facts have evolved…We now have a detailed description which, to my mind, is very much not like a faint. The description, as I understand it, is that Kurt was eating his dinner and almost without warning fell head first into his dinner. I have not encountered this in patients who faint and from the description it sounded to me as if there was not an immediate prodrome, although I obviously accept what Professor McGuire has emphasised, that he was unwell earlier in the day.”

Professor Saul also thought that the manner in which Kurt fell was significant. He said: “I think the important issue here for me in determining whether this issue was vasovagal or arrhythmia is very much related to what Mr Higgs was just talking about. Does it matter whether you fall to the side and slump to the floor or fall into your food? If we read from the prior transcript of Ken Halverson on page 44, starting at line 7, he says: ‘We had been eating the meal for a while, I can’t determine how long, and Kurt fell forward. He slumped forward and his face went into his food.’ The reason that’s important to me is that I primarily see children – and Kurt at the time was 13 and a half. I see five to 10 children a month with syncope and the reason they come to me is to rule in or out a malignant cause of their syncope. One of the primary things that I use is does somebody hurt them or do they fall into an unusual way? [sic] I have to say that I have never seen a patient who had a benign cause of syncope that fell into their food like that. It doesn’t mean it couldn’t occur. Professor McGuire said he sees a lot of adults who do that, but in my many years of seeing children – and that’s about since 1984 – I don’t think I have seen a single case in which a benign cause of syncope caused someone to fall into their food. The reason for that is the brain has a little bit of warning time with benign syncope. As the blood pressure goes down, even though people may fall, they almost never hurt themselves because the brain allows the body to get out of the way of items that they might hit, to fall a little bit softer on to the floor, to not fall face first into their food. It rarely occurs while driving for the same reason. So I think this particular issue, which was not present in the prior descriptions but we only got it when Ken Halverson told us exactly what he remembered in court, is a critical part of that event that suggests, to me, that it can’t be written off as a vasovagal or hypotensive event.”

Associate Professor McGuire gave evidence that he had seen patients on several occasions who had fallen into their food as a result of benign syncope. He was of the opinion that: “…this was a simple faint because the patient was feeling unwell all day. There was a prodrome. Typically, the arrhythmias of long QT Syndrome aren’t always associated with being unwell and vomiting. This patient felt unwell, was probably dehydrated and he fainted.”

Professor Harris substantially agreed with this view. To both himself and Associate Professor McGuire, the 1995 syncopal event was typical of a vasovagal or hypotensive incident. It occurred in the context of Kurt being generally unwell, and it was preceded by the premonitory sign of Kurt’s food tasting unpleasant. To them, there was no special significance in the way that Kurt fell. Other views

Like Associate Professor Richards, the cardiologist Dr Silberberg (who was called by the defendant as a witness of fact) came to different conclusions about the 1995 syncope depending upon which description of the event he relied upon. The following exchange occurred in his examination in chief: Q. Let’s just take it incrementally, if you wouldn’t mind. Firstly, if the description of the faint that was provided to you is as set out in this letter [i.e. Dr Wilkinson’s letter] and you had no other information – A. This is the same pattern as the others, really. Something has come on him, and then he’s said, ‘It’s not right’ and he has blacked out. Q. Are there any premonitory signs that you glean from this history? A. Yes. He has been unwell throughout the day; he did not feel like eating, he did not feel like eating lasagne.”

The description of the events given by Kurt’s father was then read to Dr Silberberg from the transcript. “Q. …Does that impact upon anything in terms of your management of the patient, if you had been provided that history in February 2001 about this September 1995 faint? A. I would have said, ‘Gee, that first one sounds like a seizure to me.’ I wouldn’t have initiated anything of my own consultation or action, but I would probably have invited a review by the neurologist, if I had that much information. The key bit there is that his dad was saying that he’s sitting, eating and, without a word, his face is in his food and then, when he wakes up, he’s aggressive…”

Although Dr Silberberg’s conclusion that the syncope sounded neurological was largely based on Kurt’s family history and the fact that he was aggressive when he regained consciousness, it is clear when Dr Silberberg said “and, without a word, his face is in his food” that on the basis of Mr Halverson’s evidence he thought that there was no clear prodromal event.

Dr Raftos was of the view that all of Kurt’s syncopal events had a cardiological cause. He did not accept that an unpleasant taste of food was a typical prodrome. The following exchange occurred in cross-examination: “Q. In relation to vasovagal events, it is well known, is it not, in the literature, that premonitory signs such as being off your food is something that falls within the rubric of a prodromal event in the way that we have discussed? A. My understanding of the prodromal features of a vasovagal faint are that you have a premonition that you are going to faint in that you start to feel woozy, you start to feel the need to sit down, you may start to sweat, but they occur within five or 10 minutes before the faint. I’m not aware of symptoms occurring at a greater distance.” The event in June 1998

I have found that the event described by Mr Ron Halverson when Kurt collapsed outside Dr Dobler’s surgery happened and was reported to both Dr Dobler and his wife. Although the event was not recorded by Dr Dobler, the circumstances were such that it is inconceivable that they were not told about it. However, probably because Kurt was suffering a significant migraine attack at the time, the significance of the collapse was not appreciated.

All of the cardiologists agreed that the 29 June 1998 syncope was most likely a vasovagal event or an episode of hypotension. The critical factor in this diagnosis was the grandfather’s report that Kurt said he was about to collapse, which is consistent with benign syncope. It was nevertheless agreed that they all would have requested an ECG at this point, although Professor McGuire qualified his agreement, stating that he would only have ordered an ECG if the 1998 syncope was unexplained. Since he believed that both events were benign, there was therefore no need to perform an ECG. All of the experts agreed that an ECG performed at this time was likely to be normal.

Given the broad consensus between the cardiologists as to the nature of the June 1998 syncopal event, I accept that it did not have a cardiogenic cause. The response to the murmur found on 1 February 2001

The cardiologists all agreed that they would have obtained an ECG following the detection of the murmur. Professor Saul and Associate Professor Richards believed that Dr Dobler should have obtained an ECG and sent Kurt to a cardiologist within 48 hours. Professor Harris and Associate Professor McGuire were of the view that referral to a cardiologist was only necessary if the ECG was abnormal or the murmur persisted. The syncopal episode of 4 February 2001

In relation to the 4 February 2001 syncopal episode, Professor Harris and Associate Professor McGuire believe the cause was more likely to be vasovagal or hypotensive. Associate Professor Richards and Professor Saul believe the cause was most likely a cardiac arrhythmia.

The former cardiologists based their opinion, in part, on the fact that Kurt had been unwell through the day, but as Professor Harris notes: “He drank the milk and the thing that sways me in favour of it being vasovagal and hypotension is that he called out to his father, indicating to me a prodrome…He actually had enough time to place the glass of milk down as he fell or as he fainted.”

Associate Professor McGuire was of the same view. However, Associate Professor Richards was of the view that this “is not a prodrome in the way that a vasovagal episode is a prodrome where the patient feels faint and then slumps. This was very, very prompt and he was promptly on the floor.” Accordingly he saw this episode as more likely to be cardiogenic.

Although Associate Professor Richards originally thought that the syncopal event of 4 February 2001 was probably vasovagal, and that it was unlikely that Kurt’s recurrent syncope was caused by any sort of arrhythmia, he altered his view in his report of 4 October 2005. In that report he stated that “the syncope of 4 February 2001 does not sound to me like a simple faint, and sounds to me more like a self terminating ventricular tachyarrhythmia.” In his report dated 24 April 2006, Associate Professor Richards stated that “it is my view that the syncope 4 February 2001 should have been considered in the context of previous syncope and presyncope, and cardiac causes for syncope (bradycardia and tachycardia) should have been considered.”

In his first report dated 11 July 2005, Professor Saul had stated that of itself the 2001 incident was typical of vasovagal syncope in the presence of a viral illness. He altered his view in his third report of 6 April 2006 where he said that the event “was atypical for vasovagal syncope, with the event occurring suddenly while drinking milk.” Professor Saul stated in court that while the event in itself was consistent with being of either vasovagal or cardiological origin, the fact that it was recurrent led him to favour the latter as the true cause. Both Professor Saul and Associate Professor Richards did not think that there was any postural element that indicated a vasovagal event or an episode of hypotension.

Dr Silberberg was of the opinion that the February 2001 syncope was clearly accompanied by a prodromal event which indicated that the syncope was vasovagal in origin. The prodromal event was Kurt’s calling out “Dad” and putting his glass of milk down before he collapsed. Dr Raftos expressed a contrary opinion. In cross-examination he stated that Kurt’s saying the word “Dad” about a second before fainting was not “typical of a prodrome of a vasovagal episode.”

All of the cardiologists also agreed that if consulted after the syncopal event in February 2001 and given the previous history of syncopal events, the detection of a murmur on 1 February and a current diagnosis of glandular fever they would have reviewed Kurt’s history, performed a physical examination and carried out an ECG. Professor Harris, Professor Saul, and Associate Professor Richards would have required in-hospital continuous monitoring regardless of what they believed was the cause of Kurt’s syncope, but Associate Professor McGuire would not have insisted on such monitoring if the history was strongly consistent with hypotension or vasovagal syncope. All of the cardiologists would have asked for an echocardiogram to be performed as soon as convenient. It was agreed that if the ECG and the monitoring were normal, monitoring would be discontinued after 24-48 hours. What would an ECG have shown?

The ultimate question in this case is whether an ECG performed at any time, but more particularly shortly after the 4 February event, would have revealed a prolonged QT interval (or other significant abnormality) and prompted a continuous care response for Kurt.

The starting point for an analysis of the difference of opinion amongst the cardiologists is to begin by setting out what they do in fact agree upon. I have already recorded that they all agreed with the following: “Long QT syndrome is a complex range of conditions. It is not a single disease with a single outcome. It can be caused by genetic factors, environmental factors or a combination of the two. Environmental factors include drugs, electrolyte abnormalities, myocardial ischaemia, brain injury, bradycardia, hypothermia and stressors which activate the sympathetic nervous system. Regardless of the cause there is a risk of death due to abnormal heart rhythms. The prevalence of the genetic condition is probably in the order of 1 in 3000 of the population. A precise diagnosis of Long QT Syndrome can be difficult to make.”

All of the cardiologists agreed that it was possible that an ECG taken at the relevant time could have revealed a long QT interval. However, they disagreed as to the likelihood that it would be revealed. They also agreed that Kurt had some form of long QT Syndrome. The critical question is whether during the period following his collapse on 4 February and the ultimate catastrophe there were environmental factors present in Kurt which could have triggered an abnormal heart rhythm that would have shown up on an ECG. This is lucidly revealed in a portion of Professor Saul’s evidence where he said: “…Professor McGuire and Professor Harris brought up a few issues of whether this is a usual or unusual case of long QT syndrome. I would say in my experience, which is fairly broad with the syndrome and particularly in children, that as Professor Richards said, it’s a variety of sympathetic stressors and sometimes no stressors and that all of these patients have intermittent symptoms. None of them have symptoms every day, every month or even every year…It is very hard to determine a specific stressor in every specific patient. It is clearly a combination of genetics and environment because when we label somebody with long QT Syndrome, again we are saying that they don’t typically have their symptoms every day; they have them under certain circumstances. … The issue in any individual patient isn’t so much what the individual stressor is, it’s what the symptom was, and syncope is the primary symptom of the long QT Syndrome that precedes any sort of malignant events. So the issue in this boy is not so much was it a viral illness. We almost know for sure in him it was a viral illness. What it is is that he had a syncopal event and the syncopal event is investigated specifically to rule out such things as the long QT Syndrome. That’s the primary reason that an ECG is obtained in somebody who has syncope. In this syndrome we know that 25 to 30 per cent of patients actually have a normal [ECG] at various times and, again, he fits well with that. We know that patients present with malignant events, and he had that. We know that they have torsades des pointes as a form of ventricular tachycardia and he had that. We know that they can have very long and abnormal long QT intervals and he had that. To me this is not an atypical case, it is not an unusual case, it is just one of the many manifestations of long QT syndrome, and if you look through the comments in both the defendant’s answers to the questions and the plaintiff’s, you will see that for the most part the plaintiff’s experts and the defendant’s experts agree that this was a form of the long QT Syndrome. It is only a question of what were the stressors that brought it out in this boy. ” (Emphasis added).

The different opinions that were expressed in relation to this issue resulted largely from the interpretation of the results of ECGs performed on Kurt after his cardiac arrest.

It is uncertain whether the first ECG performed on 11 February 2001 following Kurt’s cardiac arrest revealed a long QT interval. Professor Harris and Associate Professor McGuire thought that it did not, while Professor Saul and Associate Professor Richards thought that it did. Nevertheless, it was agreed by all four experts that this ECG was abnormal.

All of the cardiologists agree that a long QT interval was revealed on Kurt’s next three ECGs (12, 20 and 21 February). However, an ECG on 25 February was normal. Professor Saul and Associate Professor Richards attributed Kurt’s long QT interval following his cardiac arrest to the presence of congenital LQTS (exacerbated by other factors). However, Professor Harris and Associate Professor McGuire believed that the long QT interval after Kurt’s cardiac arrest was induced by environmental factors which were not present before the arrest such as the recent cardiac arrest, hypoxic brain damage with sympathetic storms, and bradycardia, with a possible genetic component. Fourteen ECGs were performed on Kurt between 11 February 2001 and 7 September 2004. On the only other occasion after 21 February 2001 where it was agreed by all the experts that an ECG revealed a long QT interval (2 July 2002), Professor Harris and Associate Professor McGuire attributed it to the presence of the drug Cisipride. However, it is notable that on at least one occasion (1 August 2003), and possibly others, Kurt was taking Cisipride but his ECG did not show a prolonged QT interval. Professor Harris and Associate Professor McGuire are of the view that on the only occasions when a long QT interval has been documented in Kurt it was documented in circumstances where even a person without LQTS could display a prolonged QT interval due to the presence of factors that are capable of inducing such an effect.

Professor Saul and Associate Professor Richards believed that there was an environmental factor present between 4 and 10 February that provoked a long QT interval, namely, Kurt’s glandular fever. I have already pointed out that all of the cardiologists agreed that “stressors which activate the sympathetic nervous system” are environmental factors that can cause a long QT interval. Professor Saul gave evidence that “certainly a viral illness is one of the things that does activate the sympathetic nervous system.” Associate Professor Richards gave evidence to the same effect. Neither Professor Harris nor Associate Professor McGuire challenged the proposition that a viral illness such as glandular fever can activate the sympathetic nervous system. Nevertheless, notwithstanding his agreement with the general statement that stressors that activate the sympathetic nervous system can cause a long QT interval, Associate Professor McGuire said that: “I see a lot of patients with abnormal heart rhythms and quite a few patients with long QT syndrome. I have never seen a single example of a case where the arrhythmias were reliably precipitated by viral illnesses. I don’t believe there is any evidence that viral illnesses cause arrhythmias in long QT syndrome.”

Professor Saul was of the view, which I accept, that the difference of opinion between the cardiologists was essentially due to the fact that as yet there is nothing in the scientific literature that says that viral illnesses specifically might lead to arrhythmias in patients with LQTS. In relation to this, he said: “To me, it doesn’t make that much difference whether we know in other people it did because…in this boy the viral illness was the stressor.”

And again, in light of what ultimately happened to Kurt, the Professor said: “We almost know for sure in him it [i.e. the stressor] was a viral illness.”

Associate Professor McGuire, on the other hand, thought that “we should confine our discussion to evidence based medicine” and was content to say that “usually the arrhythmias in this syndrome occur almost at random times” rather than draw an explicit link between arrhythmias and viral illnesses on the basis of Kurt’s case.

Professor Harris sought to draw a distinction between the academic statement about stressors that activate the sympathetic nervous system on which the experts had all agreed and his opinion as to what factors were actually operating on Kurt. He did not think that the viral illness was one of them.

Associate Professor Richards took a position that was somewhere closer to the middle ground, stating that: “There is obviously a whole host of stressors that may precipitate long QT and Professor Harris has emphasised that in some groups there may be some reproducible events, such as noise, that may precipitate an attack. Professor McGuire has indicated that it may appear to be essentially random. In this fellow, in addition to the viral illness per se, there was the question of electrolyte abnormalities and certainly sympathetic stress generally in some patients with some of the long QT syndromes have their arrhythmias precipitated by stress. I agree that I have not read in the literature a series of patients who have a viral illness per se as the sole precipitating factor.”

Although the cardiologist Dr Silberberg was called by the defendant as a witness of fact rather than as a medical expert, he agreed with the proposition that a prolonged QT interval could be associated with physical stress such as glandular fever. A passage from Schwartz et al “Diagnostic Criteria for the Long QT Syndrome: An Update” (1993) 88(2) Circulation 782 was put to Dr Silberberg, in which the authors state that Long QT Syndrome is “characterised primarily by prolongation of the QT interval and by the occurrence of life-threatening tachyarrhythmias, particularly in association with emotional or physical stress.” The following exchange then occurred: “Q. …Are you comfortable with the accuracy of that piece of learning? A. Sure. Q. Physical stress, of course, would comprehend someone who is debilitated with glandular fever, for example? A. Definitely, that covers it.”

In summary, all the specialists agree that the most likely cause of Kurt’s cardiac arrest was LQTS. They differ as to whether or not this was likely to be detected on an ECG if one had been performed between 4 and 10 February 2001. Professor Harris and Associate Professor McGuire contend that the stressor that precipitated Kurt’s cardiac arrest was either random or unknown, and that in the ECGs following the arrest a long QT interval has only ever been detected in Kurt in the presence of environmental factors that were not present in the period preceding the arrest. Consequently, they believe that an ECG between 4 and 10 February was unlikely to reveal any abnormalities. They are of the opinion that prior to Kurt’s cardiac arrest it was more likely than not that an ECG would not have revealed a prolonged QT interval. Associate Professor McGuire said: “So I would say there was a greater than 80 per cent chance that the ECG would be normal at any specific time because 80 per cent of the ECGs I have examined are normal. The only ones that are abnormal are under extreme provocation.”

Professor Harris reasoned that since an ECG performed within a matter of hours after Kurt’s cardiac arrest did not reveal “an extreme QT,” and given the presence of other factors that could explain the prolonged interval on later ECGs, “I think most likely ECGs done prior to these are highly likely to be normal, of the order of 80 or 90 per cent.”

Mr Williams SC questioned both Professor Harris and Associate Professor McGuire about their ability to assess the likelihood of an ECG revealing a long QT interval on 5 February 2001 when they each held the view that the syncopal event of 4 February was vasovagal and not cardiogenic. Professor Harris conceded that “it would be inconsistent to argue that there was a likelihood of long QT if the diagnosis was vasovagal,” but later argued that – assuming that the event was caused by an arrhythmia – an “ECG on the 5th would be back within the normal range of QT.” This view was based on a comparison with the behaviour of Kurt’s QT interval after his cardiac arrest. That is, the Professor thought that “if we assume that at the time of the arrest it [the QT interval] was very long, the QT is back within the grey zone a few hours later,” and so the same thing is likely to have happened in the first few hours following a syncopal event caused by an arrhythmia. The Professor conceded that this view was based on “fairly thin” scientific data.

Professor Saul and Associate Professor Richards approach the matter differently to Professor Harris and Associate Professor McGuire. They are of the view that a viral illness can precipitate an arrhythmia in people with LQTS, and that this in fact happened to Kurt. In their opinion there were no other stressors present that were significant enough to have provoked an arrhythmia in Kurt (although there were some, like mild electrolyte abnormalities, that may have made some contribution), and that the viral illness was the only stressor present during both the 4 February and the 11 February malignant events. Professor Saul noted that “25 to 30 per cent of the patients with congenital long QT Syndrome have a normal QT interval on at least some ECGs.” He also noted that “syncope is the primary symptom of the long QT Syndrome that precedes any sort of malignant events.” Since Professor Saul and Associate Professor Richards believed that the syncopal events on 4 September 1995 and 4 February 2001 (but not the event on 29 June 1998) were manifestations of Kurt’s LQTS (i.e. they believed that the faints were due to cardiac arrhythmias rather than of a vasovagal origin), they were confident that ECGs taken around the time of these events would have revealed a long QT interval. Professor Saul said: “It seemed to Professor Richards and I that around the time of the syncopal events he was most likely to have a long QT because he was manifesting a symptom of the disease.”

Associate Professor Richards rated the chance of finding a long QT interval after 4 February 2001 as “a very high probability, more [than] 50 per cent at least.” Professor Saul rated the chance as “very likely.” Dr Raftos, who also believed that the 4 February incident had a cardiological cause, stated in his report of 24 March 2006 that ECGs performed on 4 and 5 February would, on the balance of probabilities, have revealed a long QT interval.

During the course of the discussion during concurrent evidence Professor Saul gave an explanation for the difference of opinion between the cardiologists. He thought that the position of Professor Harris and Associate Professor McGuire was based on an overall assessment of the 14 ECGs that had been recorded for Kurt between 11 February 2001 and 7 September 2004. Taking that longer view would indicate that 4 of 14 ECGs showed a long QT interval. Working backwards from this figure, they felt that the chances of an ECG revealing a long QT interval between 4 and 10 February would accordingly be low. On the other hand, Professor Saul and Associate Professor Richards took a more narrow view of the incident, confining their assessment largely to the ECGs recorded in the period immediately following the cardiac arrest (the “peri-event period”). On this basis, 3 out of 4 (according to Professor Harris and Associate Professor McGuire) or 4 out of 4 (according to Professor Saul and Associate Professor Richards) of the ECGs recorded between the time of the arrest and 21 February revealed a long QT interval. Working backwards from this information, and having regard to the fact that Professor Saul and Associate Professor Richards believed the 4 February syncope to have been caused by an arrhythmia relating to Kurt’s LQTS, they thought that the chances of an ECG revealing a long QT interval between 4 and 10 February was accordingly very high. Professor Saul summarised the differences of opinion in this manner: “We pretty much decided [during the joint conference] that it is [long QT syndrome that caused Kurt’s cardiac arrest], but on the case of Professors McGuire and Harris that it was an unusual case with certainly [sic] unclear precipitators and for the case of Professor Richards and myself that it is not as unusual a case with probable stressors of the viral illness aspect.”

The following exchange between Associate Professor McGuire and Professor Saul is instructive: “Prof McGuire: As we have both agreed previously, patients with long QT Syndrome can have arrhythmias without any of these factors [i.e. the environmental factors recognised in the literature as provoking a long QT interval] being present. You are postulating a new factor that hasn’t been documented in the literature previously: would you agree with that? Prof Saul: No, I wouldn’t agree because in the literature sympathetic stressors are what is talked about and I believe if you looked at any of the databases you would see that sometimes there were viral illnesses, but to me it doesn’t matter because we only have the viral illness in [Kurt]. We don’t have electrolyte abnormalities. We don’t have any significant drug effects. We don’t have myocardial ischaemia. We don’t have brain injury prior to the arrest. We don’t have significant bradycardia. We don’t have hypothermia. The only thing we have is the stress of his current viral illness and his history is such that all of his events occurred during viral illnesses.”

Apart from Kurt’s viral illness, as I have indicated there were other factors present between 4 and 10 February that could have contributed to a long QT interval in Kurt. All the cardiologists agreed that certain drugs, electrolyte abnormalities, and bradycardia could cause a long QT interval. There is evidence that all three of these factors were likely to have been present to some degree in Kurt during the relevant time.

In relation to the presence of drugs that could provoke a long QT interval, the following exchange occurred: “Professor Saul: Were there any drugs that would cause arrhythmias such as torsades des pointes [at the time of Kurt’s cardiac arrest]? Professor McGuire: A couple of days before the episode there were the two drugs, Promethazine and Prochlorperazine, which we know can precipitate arrhythmias in long QT syndrome. Professor Saul: I think we all agreed last night that those were probably cleared significantly from the bloodstream at that point. Professor McGuire: I am not sure that we can be certain about that…”

Dr Raftos said in his report of 24 March 2006 that “it is possible that the phenergan and [stemetil] with which [Kurt] was treated also contributed to the prolongation of the QT segment that precipitated” his cardiac arrest. Dr Raftos gave evidence that, as is recorded in the product information sheet published by the makers of Stemetil, some of the known adverse reactions to therapeutic doses of Stemetil (more correctly, the drug Prochlorperazine) are QT prolongation, torsades de pointes and sudden death. It has been known since 1995 that Stemetil can prolong the QT interval. It appears from the hospital notes that Phenergan (or Promethazine) was given to Kurt on 7, 8 and 9 February 2001, and Stemetil was administered on 8 and 9 February 2001.

In relation to the electrolyte abnormalities revealed in the hospital records, all of the cardiologists accepted that they were mild. It was agreed that while they would not have caused an arrhythmia on their own they could have contributed to an arrhythmia.

Lastly, there is the issue of Kurt’s bradycardia. Dr Dobler was cross-examined in relation to this issue (bradycardia occurs when the pulse rate is below 60 beats per minute): “Q. To summarise those, between 9.30pm on 4 February and 2pm on 5 February, there is evidence of the pulse being recorded on 10 occasions? A. Yes. Yes, that’s correct. Q. And the range is from 60 down to 40? A. It would appear so, yes. Q. And most, that is 7 out of 10, are below 50? A. It’s hard to judge. Certainly a good proportion were below 50. … Q. …But that overall picture between the 4th and 5th is one of bradycardia, is it not? A. That’s correct.”

Additionally, Kurt’s pulse was below 60 on roughly half of the occasions on which it was recorded during his admission to Hospital between 7 and 10 February 2001.

I have previously indicated that all of the cardiologists agreed that if an ECG performed on or before 5 February had revealed an abnormality, they would have required Kurt to be placed under continuous monitoring. Associate Professor McGuire qualified his answer by saying that he would only order continuous monitoring if the abnormality was significant (such as a long QT interval) rather than a minor or non-specific one. It was agreed by all the Professors that if an ECG or monitoring after 5 February 2001 had revealed an abnormality, monitoring would have continued until definitive therapy was established. If the monitoring and an ECG were normal, monitoring would have only continued for 24 to 48 hours.

All four cardiologists agreed that Kurt had LQTS, but they characterised it differently. Professor Harris and Associate Professor McGuire described it as an atypical case of a genetic propensity for LQTS exacerbated by environmental factors. Professor Saul and Associate Professor Richards classified it simply as a case of congenital LQTS. All of the cardiologists agreed that Kurt’s LQTS was the most likely cause of the ventricular fibrillation on 11 February 2001, but that Epstein-Barr myocarditis or an unknown cause could not be excluded. They also agreed that Kurt’s heart murmur was not related to his LQTS or to myocarditis. They thought it was probably a flow murmur associated with Kurt’s viral illness and that it probably was not a pansystolic murmur.

Associate Professor McGuire pointed out that even if an ECG had been performed, and even if it had revealed a prolonged QT interval, there might be an issue as to: “whether Dr Dobler would have identified it as being abnormal, and whether that was reasonable for a general practitioner to do that. Even if he had referred to another cardiologist, I note that several cardiologists did not make the diagnosis, so there is still a significant chance that even if Mr Halverson had been referred to a cardiologist, the diagnosis would not have been detected and the catastrophe may still have occurred.”

The ECG at Cessnock Hospital was a self-interpreting machine that automatically measured the QT interval. Dr Dobler, an experienced medical practitioner and VMO at the hospital, was required to use the ECG as a diagnostic tool. Although I understand that identifying a long QT interval on the ECG may require some skill, Dr Dobler did not suggest he could not identify it. If evidence of a long QT interval was present on the ECG trace I am satisfied, on the balance of probabilities, that Dr Dobler would have identified it. The medical literature

The parties tendered a significant volume of relevant medical literature.

Three works were singled out by the general practitoners as being available and directed to Australian general practitioners. The first was an article by Daroff et al that is contained in the 1998 edition of Harrison’s Principles of Internal Medicine . It states that where a patient presents with syncope and the history and physical examination are normal, the diagnosis should be vasovagal or hypotensive syncope. It is noted that vasovagal syncope is usually precipitated by specific triggers (such as the sight of blood or receiving an injection), and hypotensive syncope is usually associated with a change in posture. In “most instances, fainting is relatively benign. In dealing with patients who have fainted, the physician should think first of those causes of syncope that constitute a therapeutic emergency. Among them are…cardiac arrhythmias” (p 104). It is noted that Holter monitoring is warranted where a cardiac cause is suspected.

The second work was a chapter titled “Faints, fits and funny turns” in the 1998 edition of Murtagh’s General Practice . The approach recommended by Murtagh was dealt with extensively in the oral evidence of the GPs, and placed a heavy emphasis on adequate history taking on presentation. It was stressed that cardiac causes of syncope are often overlooked and should not be missed.

The third work was an article by Barlow and Leitch that appeared in a 2004 issue of Australian Doctor . It emphasised that only in “occasional” cases would a history be sufficient to lead to a positive diagnosis of a syncopal event. An example given was when a person faints at the sight of blood. In all other cases, an ECG is indicated “because it gives evidence of…a variety of uncommon electrical disturbances capable of causing sudden death” (p 38). Nevertheless, the authors observed that, due to the transient nature of cardiac arrhythmias, the chances of detecting one on an ECG or on Holter monitoring was relatively low. In this regard, it should be pointed out that a prolonged QT interval is not usually itself referred to as an arrhythmia; however, when it is revealed on an ECG it indicates that a patient may be predisposed to arrhythmic events.

There is no uniform approach in the literature to diagnosing vasovagal or hypotensive syncope. Some state that a history and physical examination will usually be enough to ground a positive diagnosis, while others hold that an ECG is also essential before a diagnosis can be made. In the 1998 edition of Family Medicine Principles and Practice , MacDonald states that vasovagal syncope is diagnosed by ruling out other causes, whereas in the 1996 edition of Heart Disease Diagnosis and Therapy – A Practical Approach, Khan says that “in patients with [vasovagal] syncope, the diagnosis can be made in virtually all patients from a relevant history and physical” (p 535). What is clear from all sources, however, is that since the cardiac causes of syncope have a catastrophic potential, they must be considered in any patient who presents with syncope. It is also clear that a history and physical examination will only be sufficient to exclude cardiac causes where the history indicates that the syncope was accompanied by a specific trigger (such as the sight of blood, emotional stress, receipt of an injection, pain, or prolonged standing in the sun or in crowded confines), or with a change in posture. In the absence of these factors, the most likely diagnosis might still be vasovagal or hypotensive syncope, but this cannot be diagnosed with certainty. It is noted by Pedley et al in the 1995 edition of Merritt’s Textbook of Neurology that “[c]lues to cardiac origin for syncope include attacks with little relation to posture, position, or specific triggers” (p 16). If there is any suspicion that the syncope is not benign, basic investigations (beginning with an ECG if one has not already been performed) will need to be undertaken at this point. When syncope is recurrent, the need for an ECG becomes even greater.

The literature also deals with the question of what an ECG is likely to reveal following an episode of syncope. It is widely accepted that due to the transient nature of arrhythmias, an ECG following an arrhythmic syncope may be normal. Hence, a longer period of Holter monitoring may be necessary. Arrhythmias found on Holter monitoring will not be etiologically significant unless they occur while the patient is simultaneously displaying symptoms (e.g. by losing consciousness), but they may reveal arrhythmias that will warrant investigation in and of themselves. Again, it should be stressed that the likelihood of finding an arrhythmia is not the same as the likelihood of finding a prolonged QT interval. As Boudoulas et al note in the 2001 edition of Hurst’s The Heart , “because of the transient nature of most arrhythmias, the routine ECG is generally of limited value. It is, however, very useful in identifying patients with abnormalities that may predispose individuals to syncope” (p 1005). A long QT interval is an abnormality that may predispose individuals to syncope.

A 1993 study by Garson et al, titled “The Long QT Syndrome in Children,” is of especial relevance to this case. It involved 287 children (under 21) who presented with unexplained syncope, seizures or cardiac arrests, or with a family history of LQTS. Seventeen children had a normal QT interval (i.e. a QTc of less than 0.44) at presentation. It was found that “Among all 17 patients with normal QTc at presentation, in three, the QTc was found to be more than 0.44 at follow-up; each of these was 0.46 or more. All three of these patients had serious symptoms [serious symptoms were defined as cardiac arrest, syncope, or seizure] or sudden death at follow-up, whereas none of the patients in whom the QT remained at less than 0.44 had either symptoms or sudden death at follow up” (p 1869). To my mind this is very significant, given that Kurt does not consistently have a long QT interval on an ECG. This study indicates that in patients who do not always manifest signs of LQTS, an ECG subsequent to LQTS associated symptoms such as syncope is likely to record a long QT interval. This is significant if the syncopal event of 4 February was caused by an arrhythmia that was a manifestation of Kurt’s LQTS, particularly in light of the fact that a long QT interval was arguably recorded in the first ECG taken after Kurt’s cardiac arrest (in any event, it was agreed that this ECG was “abnormal”), and a long QT interval was definitely recorded in his next three ECGs.

It is apparent from the literature that in LQTS malignant events are usually precipitated by specific triggers. The most common triggers are exertion or emotional stress. As Vincent notes in “Heterogeneity in the Inherited Long QT Syndrome” (1995) 6(2) Journal of Cardiovascular Electrophysiology 137 at 143, “The classic symptom of the syndrome is syncope/sudden death occurring during exercise, fear, sudden noises, or other emotional stress.” What these triggers have in common is that they activate the sympathetic nervous system, which led Schwartz to conclude in 1985 that “The strong association between the syncopal episodes and physical or emotional stress has constantly pointed to a critical role of the sympathetic nervous system in the genesis of the malignant arrhythmias typical of LQTS” (“Idiopathic Long QT Syndrome: Progress and Questions” (1985) 109 Am Heart J 399 at 404). This is consistent with the views expressed by the cardiologists in this case, whose difference of opinion largely comes down to whether Kurt’s viral illness (which could have activated his sympathetic nervous system) precipitated the two syncopal events that occurred in February 2001. Resolving the question

It is a difficult task for a court to resolve the difference of opinion between four highly qualified, experienced cardiologists each of whom was in my opinion endeavouring to provide the court with the benefit of their learning and experience. If the matter was able to remain a purely scientific debate the differences of opinion may be documented and the problem could remain unresolved. However, the law requires a resolution, although the plaintiff carries the legal onus of proving his or her case: T C (by his tutor Sabatino) v The State of NSW & Ors [2001] NSWCA 380.

In any medical negligence case there is always a risk that the impact of the revealed tragedy will colour the analysis of the preceding events and any finding as to the standard of care and breach of duty. As Ipp JA observed in Capital Brake Service Pty Ltd v Nicholas Kevin Meagher & 8 Ors t/as Sparke Helmore [2003] NSWCA 225 at [30]: “There is a great danger, particularly in professional negligence matters, of applying an unrealistic hindsight judgment. Any fool can be wise after the event. That is not the test. The Court must be careful to judge the conduct of a defendant, where a negligent failure to warn is asserted, by reference to what the defendant reasonably knew at the relevant time. Not after the loss has been suffered.”

The cardiologist Dr Silberberg was well aware of the problems posed by hindsight when during the course of his evidence he spoke of the “retrospectoscope.” “Q. Exactly, doctor. Indeed, the general practitioner is the captain of that ship [i.e. responsible for diagnosis], is he not? It is his patient. A. When I say I don’t see my job as diagnosis, I’m not saying I won’t take responsibility. I’m saying that my job is to comfort the – sometimes you have to live with doubt. A lot of my practice is reassuring people that, thus far, things have gone quite well and therefore we don’t have to panic. Clearly, with the retrospectoscope, I would have been wrong in Kurt’s case. But, yes, the general thing that you are putting to me, axiomatic as it is, that we do our best to exclude the serious and make the diagnosis of the alternative, is right. That is what we do. His Honour: Q. Just before we break, what do you mean when you say that with the retrospectoscope, you would have been wrong? A. Because Kurt had a bad outcome. I would have been reassuring until even 10 February, on the way that – as I sit and experience this thing - Q. I am just trying to work out what is the error that you recognise. You say you were wrong. I assume that that imputes some error that you would have made. Can you help me? Is that the right way to understand what you said? A. Well, he was about to have a cardiac arrest, and I would have been reassuring that this was not even a cardiac presentation. I would have seen – it is most unlikely. I would have reassured him that there is almost no risk, and I would have been wrong, because it turned out he did.”

The role of hindsight in the law of negligence has recently been considered by Hayne J in two recent High Court judgments ( Neindorf v Junkovic (2005) 222 ALR 631 at 654-656; Vairy v Wyong Shire Council (2005) 223 CLR 422 at 460-462). In the latter case his Honour points out that while it is entirely appropriate to use hindsight to look at the issue of causation, the question of breach of duty must be approached prospectively. At 743 his Honour says: “the examination of the causes of an accident that has happened cannot be equated with the examination that is to be undertaken when asking whether there was a breach of a duty of care which was a cause of the plaintiff’s injuries. The inquiry into the causes of an accident is wholly retrospective. It seeks to identify what happened and why. The inquiry into breach, although made after the accident, must attempt to answer what response a reasonable person, confronted with a foreseeable risk of injury, would have made to that risk” (emphasis in original).

In the present case any risk of inappropriate use of hindsight is confined to whether or not Dr Dobler should have carried out an ECG after Kurt’s collapse on 4 February 2001. That judgment must be made in light of Dr Dobler’s knowledge of Kurt’s prior history of collapse, the fact that a neurological impairment had previously been negatived, the fact that in the periods from 4 to 5 February and 7 to 10 February Kurt was in hospital where ECG facilities were easily and immediately available, and the fact that a murmur of cardiological significance had recently been identified.

The cardiological issues, on the other hand, relate to causation rather than breach. The two critical questions are whether an ECG would have revealed an abnormality and, if so, would the response have avoided Kurt’s catastrophic brain damage. The answers to these questions are informed by matters known before and after Kurt’s cardiac arrest. With respect to the second matter there is effective agreement. The first matter I have resolved after a careful consideration of all the evidence, in particular the differing views of the cardiologists.

I am satisfied on the balance of probabilities that Kurt has long QT syndrome and it was this which caused the cardiac arrest which struck him on the early morning of 11 February. Although he suffers from the syndrome it is not a condition which is always present and, even if present, may not lead to a cardiac arrest. Most probably, some physical or environmental stressor will cause the QT interval to deviate from the norm. Although the stressor in Kurt could have been random I am satisfied that in Kurt’s case it was related to his physical condition at the time. He was suffering from Epstein-Barr virus (of a sufficient degree to require hospitalisation), with an imbalance in his electrolytes caused, in Associate Professor McGuire’s words, by “vomiting and dehydration and onset of illness.” There may also have been a contribution from his ingestion of potentially detrimental drugs.

As I have related, following Kurt’s cardiac arrest 14 ECGs were taken between 11 February 2001 and 7 September 2004. It is correct, as Professor Harris and Assoc Professor McGuire point out, that only 4 or maybe 5 out of the 14 showed a long QT interval. It was fundamentally for this reason that they were of the view that an ECG prior to 11 February would not have been likely to reveal a cardiac problem and rated the possibility as no greater than 20%. Associate Professor McGuire made this plain when he said that “there was a greater than 80 per cent chance that the ECG would be normal at any specific time because 80 per cent of the ECGs I have examined are normal ” (emphasis added). I note that even if this reasoning is sound, the arithmetic is wrong. On the view least favourable to the plaintiff, 4 of 14 ECGs revealed a long QT. This would equate to roughly a 28.57% chance that Kurt’s ECG would be abnormal at the relevant time. On the most favourable view, 5 of 14 ECGs revealed a long QT interval. This equates to about a 35.71% chance that an ECG would be abnormal at the relevant time. Professor Saul points out that although there is doubt as to whether the ECG on 11 February shows long QT it is agreed that those taken on 12, 20 and 21 February reveal a prolonged QT interval. Kurt had by this time, of course, experienced a cardiac arrest and hypoxic brain injury but it is reasonable to assume that he remained, as Professor Saul concluded, infected with glandular fever.

I am satisfied that the syncopal episode of 4 February 2001 and the cardiac arrest of 11 February 2001 were related. The very fact of the cardiac arrest gives the 4 February event a more sinister aspect. The fact that this was a repeated syncopal event strengthens this conclusion, particularly in light of Professor Saul’s uncontradicted evidence that recurrent syncope is “the primary symptom of the long QT Syndrome that precedes any sort of malignant events.” Although I accept the view of all the cardiologists that the 1998 syncopal event was probably of vasovagal origin, I am satisfied that the other two syncopal events were not benign. This is especially so in relation to the event of 4 September 1995, where there had been no change in posture and no clear premonitory sign. Kurt’s complaint that his food tasted unusual is consistent with his having been ill throughout the day. The fact that he fell face first into his food indicates that the syncope was sudden and unexpected. The event of 4 February 2001 is not so clear, but I accept the view of Professor Saul and Associate Professor Richards that it was the result of an arrhythmia. Accordingly, as I am satisfied that the events of 4 September 1995, 4 February 2001 and 11 February 2001 all had a cardiogenic cause. Given that Kurt had LQTS, in my opinion it is probable that the common factor which was present on each occasion – namely, a viral illness – precipitated each event. As Kurt was suffering from a viral illness continuously between 4 and 10 February, I am satisfied that it is probable that an ECG performed between 4 and 10 February 2001 would have revealed his long QT.

As I have already stated, Professor Harris and Associate Professor McGuire assess the likelihood of an abnormality being revealed on an ECG at the relevant time as being very low. Their premise is that on the occasions when a long QT interval has actually been detected in Kurt, it has been in the presence of environmental factors (recent cardiac arrest, hypoxic brain injury with sympathetic storms, bradycardia and, in 2002, the drug Cisipride) that were not present in the days leading up to Kurt’s cardiac arrest. This premise falls away once it is accepted that Kurt’s viral illness was a precipitating environmental factor, because it was a factor that was present before the syncope of 4 February and which was still present in the period immediately after his cardiac arrest when all but one of Kurt’s abnormal ECGs were recorded. To repeat again the view of Professor Saul: “…my opinion is that it is the stress of the viral illness that both caused the long QT interval and the arrhythmic event and it was much less the effect of the brain damage and cardiac arrest because, as I’ve mentioned, I see that a lot in children without QT prolongation I would say the vast majority of the time. For me the whole period from February 1 to February 21 is a period of viral illness which has exacerbated this boy’s long QT Syndrome and that’s where the likelihood comes from.”

Even if I am wrong to accept this view, the combination of bradycardia, electrolyte abnormalities and long QT provoking drugs that were each present in Kurt at one time or another from 4 February to 10 February may have had the effect that an ECG performed at this time would have revealed an abnormality.

This case again illustrates the different nature of proof on the balance of probabilities and proof to a scientific standard. As Priestley JA stated in State of NSW t/a NSW Department of Agriculture v Allen [2000] NSWCA 141 at [3]: “The two kinds of proof are quite different in their objects and methods, but are frequently the cause of confusion when medical issues are concerned. In many such cases, experts in the field of the relevant medical science give evidence of their expert opinion concerning the medical issue. Trained in the scientific method of proof, some such experts find difficulty in adjusting themselves, when giving evidence in court, to the lesser requirements of legal proof…An expert who gave evidence for a party in litigation where there has been an adverse result reached by application of the legal standard of proof is quite likely to advise the party that the result is an unscientific and unsound one.”

The tension between legal and scientific proof is apparent in this case, where Professor Harris and Associate Professor McGuire were not prepared to recognise a viral illness as an environmental factor capable of precipitating a long QT interval because it had not been recognised as such in the scientific literature. I, on the other hand, have found on the balance of probabilities that Kurt’s viral illness was a precipitating factor. My decision (although it is certainly consistent with the opinions of Professor Saul and Associate Professor Richards) is based on the evidence in the case – both lay and expert – taken as a whole. It was recognised by a majority of the Supreme Court of Canada in Faferrière v Lawson [1991] 1 SCR 541 at [159] (Gonthier J; Lamer, L’Hereux-Dube, Sopinka, Cory and McLachlin JJ agreeing) that: “Cases in which the evidence is scarce or seemingly inconclusive present the greatest difficulty. It is perhaps worthwhile to repeat that a judge will be influenced by expert scientific opinions which are expressed in terms of statistical probabilities or test samplings, but he or she is not bound by such evidence. Scientific findings are not identical to legal findings…Both this Court and the Quebec Court of Appeal have frequently stated that proof as to the causal link must be established on the balance of probabilities taking into account all the evidence which is before it, factual, statistical and that which the judge is entitled to presume” (emphasis in original; references omitted).

This is consistent with Australian authority. Dixon CJ and McTiernan, Kitto, Taylor and Windeyer JJ considered a similar problem in Ramsay v Watson (1961) 108 CLR 642 at 645. Although their Honours were there dealing with a jury trial, their judgment applies equally to myself in the present case. Their Honours said (at 645): “That some medical witnesses should go into the witness box and say only that in his opinion something is more probable than not does not conclude the case. A qualified medical practitioner may, as an expert, express his opinion as to the nature and cause, or probable cause, of an ailment. But it is for the jury to weigh and determine the probability. In so doing they may be assisted by the medical evidence. But they are not simply to transfer their task to the witnesses. They must ask themselves ‘are we on the whole of the evidence satisfied on the balance of probabilities of the fact?’”

This is a case where the issue of causation simply cannot be answered with scientific certainty. However, proof in a legal context is governed by considerations of legal responsibility rather than by the establishment of scientific absolutes. Legal causation is established by the application of common sense to the evidence as a whole ( March v E & M H Stramare Pty Ltd (1990) 171 CLR 506 at 509). This may not yield the same results as the application of the scientific method, but it provides an appropriate resolution of problems where the inherent uncertainty of human affairs may compel the scientific mind to suspend judgment. Breach of Duty

In Rogers v Whitaker (1992) 175 CLR 479 the High Court made it clear that at common law the standard of care to be applied in medical negligence cases is a question of law to be decided by the court. The question is not whether the defendant’s conduct accords with the practice of the medical profession or some part of it (although this will no doubt be a relevant consideration), but whether the conduct meets the standard of care demanded by the law. The majority (Mason CJ, Brennan, Dawson, Toohey and McHugh JJ) said at 483: “The law imposes on a medical practitioner a duty to exercise reasonable care and skill in the provision of professional advice and treatment. That duty is a ‘single comprehensive duty covering all the ways in which a doctor is called upon to exercise his skill and judgment’; it extends to the examination, diagnosis and treatment of the patient and the provision of information in an appropriate case. It is of course necessary to give content to the duty in the given case. The standard of reasonable care and skill required is that of the ordinary skilled person exercising and professing to have that special skill…” (references omitted).

They went on to note (at 489) that: “ Whether a medical practitioner carries out a particular form of treatment in accordance with the appropriate standard of care is a question in the resolution of which responsible professional opinion will have an influential, often a decisive, role to play…” (emphasis in original)

This position has been affected by statute. The Civil Liability Act 2002 (NSW) defines negligence in s 5 as a “failure to exercise reasonable care and skill.” Section 5O provides that: “(1) A person practising a profession ("a professional") does not incur a liability in negligence arising from the provision of a professional service if it is established that the professional acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice. (2) However, peer professional opinion cannot be relied on for the purposes of this section if the court considers that the opinion is irrational. (3) The fact that there are differing peer professional opinions widely accepted in Australia concerning a matter does not prevent any one or more (or all) of those opinions being relied on for the purposes of this section. (4) Peer professional opinion does not have to be universally accepted to be considered widely accepted.”

Conflicting submissions were made as to the effect of s 5O. The defendant argued that the section (which is titled “Standard of care for professionals”) sets the standard of care to be applied in all professional negligence cases. On this view, in order to establish negligence the plaintiff must prove that the provision of professional service by the defendant was not widely accepted in Australia by peer professional opinion as competent professional practice. The plaintiff submitted that s 5O is more properly characterised as a special defence that applies in professional negligence cases. Accordingly, the standard of care is still the standard that was endorsed in Rogers v Whitaker , but if a defendant is found to be negligent under this standard he or she can avoid liability if they can establish that they acted in a manner which was widely accepted in Australia by peer professional opinion as competent professional practice. The plaintiff submitted that the effect of this was that: “the evidential obligation of demonstrating that a particular manner of practice is widely held by peer professional opinion to be competent professional practice must fall upon the person seeking to take advantage of the defence, namely the professional who is alleged to have acted negligently. If, at the end of the case, the court is left in doubt about whether it has been ‘established’ that the defendant professional acted in a manner which was ‘widely accepted…by peer professional opinion’ to be competent professional practice, that simply means that the statutory defence is not made out, and the court would go on to decide the matter in the way that it would in the absence of s 5O. Of course, it may be that the court would still reach the conclusion that the professional was not negligent, in considering all of the expert evidence and drawing its own conclusions as to the appropriate standard of care, but that would not be as a consequence of s 5O. … In short, the Plaintiffs submit that the court should assess all of the expert evidence before it, as to the proper practice of a GP in the present case, on its own merits. If the evidence were simply insufficient to found a conclusion that the Defendant was negligent, then a verdict for the Defendant would be entered, and nothing need be said about s 5O. On the other hand, if the evidence were to show that there were differing bodies of opinion amongst the expert witnesses about whether the actions of the Defendant demonstrated a lack of competent practice as a GP in the critical actions and omissions relied upon by Kurt as causative of his loss, and the court were more persuaded that the body of opinion supporting a finding of negligence represented the better view of proper practice in relation to those critical actions and omissions, it would still be necessary to consider whether the alternative less-preferred body of opinion is nonetheless ‘widely accepted…by peer professional opinion’ as competent practice for a GP.”

There is little guidance to be found in relation to s 5O in the authorities. The section is mentioned briefly and inconsequentially in Ambulance Service of NSW v Worley [2006] NSWCA 102 at [38], and there does not appear to be any other case in which the section has been considered. Both the plaintiff and the defendant supported their arguments in relation to s 5O by referring to the Ipp Report ( Review of the Law of Negligence , October 2002), and the defendant had regard to the relevant Second Reading Speech and explanatory memorandum.

In my view the section is intended to operate as a defence. The section is expressed so that “a person practising a profession… does not incur a liability in negligence ” if a certain state of affairs can be “established.” The italicised words go to the issue of liability, not to the issue of negligence, although in my view this is of little consequence. There is force in the plaintiff’s submission that the fact that the test is expressed in the negative indicates that Parliament did not intend to effect a more radical change in the standard of care to be applied in professional negligence cases.

The defendant’s argument that s 5O forms part of the definition of negligence in actions against professionals is based for the most part on the fact that the section is titled “standard of care for professionals.” Under the Interpretation Act 1987 (NSW), section headings are not to be taken as constituting part of the Act in which they appear (s 35(2)). They are extrinsic materials to which a court may have regard (s 34(2)(a)). However, I am satisfied that it is not necessary to resort to extrinsic material in this case. In any event the section heading must give way to the clear words of the section.

Dr Dobler did not adequately respond to the detection of what he himself believed was a mitral-type 2/6 pansystolic heart murmur radiating to the axilla. All of the general practitioners agreed that if Dr Dobler believed what he had recorded in his notes about the murmur, then the appropriate response was to obtain an echocardiogram. But most importantly, Dr Dobler fell short of the requisite standard of care in his response to the syncopal event on 4 February 2001. By that time Kurt was in the grip of an acute viral illness, with a recently detected heart murmur which had not been explained, and was admitted to hospital following his third syncopal event associated with other illnesses in 6 years.

While I am satisfied that the second syncopal event (i.e. the 1998 incident) was in fact vasovagal, Dr Dobler’s contemporaneous records indicate that he did not reflect on other possibilities. He should have. While recurrence does not itself make a syncopal event more or less likely to be benign, it does make it necessary to investigate the cause of the event. This is because if the cause is not benign, a sinister and potentially catastrophic cause is repeatedly operating on the patient. An ECG is one of the quickest, most basic and most readily available cardiological investigations, and it is one of the cornerstones of diagnosing recurrent syncope. When Kurt suffered a third syncopal event in 2001, an ECG ought reasonably to have been performed.

Dr Raftos was of the view that an ECG should be performed whenever a person who has suffered a syncopal attack is brought to a doctor or to an emergency department. Each of Kurt’s syncopes were brought to Dr Dobler’s attention, and Dr Dobler treated Kurt in Cessnock Hospital after each occasion. Even if the view of Dr Raftos should be considered over-cautious at the time of Kurt’s first syncopal event, this probably cannot be said of Kurt’s second event. It certainly cannot be said of his third episode of syncope.

Even so, Dr Dobler will not be liable having regard to s 5O of the Civil Liability Act 2002 if it is established that when he failed to obtain an ECG he “acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice.” I am not satisfied, on the evidence before me, that this has been established. There is a clear division of opinion among the general practitioners in this case, but that would not prevent Dr Dobler from being able to rely upon the opinion of experts favourable to him, if that opinion is widely held (s 5O(3)).

I am satisfied that to the extent that the opinions of the general practitioners called by the defendant differed from those of the plaintiff, this has resulted from inappropriate assumptions about the facts (for instance, that Dr Dobler could not have believed that he had detected a 2/6 pansystolic murmur), considering the significant events in Kurt’s medical history in isolation, and a reluctance to recognise that when Dr Dobler saw Kurt on 5, 8, 9 and 10 February it was in hospital where an ECG could have been obtained with ease. I do not think that it has been established that it is widely accepted as competent professional practice when a boy is hospitalised following a third episode of syncope, in the presence of a viral illness and recently detected heart murmur, to only treat the viral illness and not investigate the syncope or perform basic cardiological investigations. As Dr Raftos pointed out: “…this isn’t complex specialist or sub-specialist medicine. This is very simple medicine. The patient presents with a syncopal episode, simple tests to exclude cardiac disease, including electrocardiogram. It’s not complex medicine, it’s very common medicine that primary care people, GPs and emergency departments, practice every day or every week and it doesn’t require any specific technology or any specific specialist knowledge”

In her evidence, Dr Chambers said that on 5 February 2001 it would have been “irrational” not to perform further cardiological investigations. She said: “It is irrational to not do this. We have had a history building up over time. We know that there is the possibility of these serious problems that are associated with syncopal attacks. The man is in hospital and we have had a cumulative history of funny turns that are not really properly explained. We have negative neurological investigations. We have a further funny turn, be it seizure, be it faint, be it drop attack – whatever it is. The man is in hospital, he has easy access to do all of the appropriate investigations.”

Although it is unnecessary to make a finding of irrationality, Dr Chambers’ evidence is significant. In my opinion, s 5O cannot relieve Dr Dobler from liability. Loss of a chance – the decision in Rufo v Hosking

The plaintiff advanced his case on alternative bases. It was submitted that if he could demonstrate, on the balance of probabilities, that Dr Dobler had breached his duty of care and caused his injuries he should recover the full amount of the sum agreed between the parties. However, as an alternative he submitted that if he persuaded the court that Dr Dobler breached his duty of care but failed to persuade the court that, on the balance of probabilities, that breach was the cause of his damage he was nevertheless entitled to recover damages, being the value of the chance lost that he would have had a successful outcome if an ECG had been performed. Although the defendant rejected this alternative submission, the response was that if the matter was appropriately resolved by determining the value of the chance lost and if the chance was greater than 50% but less than 100%, the plaintiff should be awarded damages according to that percentage of the total sum agreed.

I have found that Dr Dobler should have requested an ECG shortly after the 4 February 2001 syncopal event. It may be, as the plaintiff argued, that cardiac investigation should have been initiated at an earlier point in time, the options being at the time of previous syncopal events. However, the evidence as to the symptoms which Kurt was suffering and the evidence as to the appropriate response from a general practitioner does not enable me to make such a finding. As I have explained the position is quite different on 4 February 2001 or shortly thereafter.

The plaintiff’s evidence by which the chance of finding an abnormality on an ECG may be quantified came from Associate Professor Richards and Professor Saul. Their evidence in this regard has been set out earlier in this judgment. They did not put a percentage figure on the chance, but were of the view that it was well over 50%. Associate Professor Richards described it as “a very high probability,” while Professor Saul used the terms “very likely” and “extremely high” likelihood.

The plaintiff relied on the decision of the Court of Appeal in Rufo v Hosking [2004] NSWCA 391. In that case the plaintiff was diagnosed in early January 1992 to be suffering from systemic lupus erythematosus, a serious inflammatory condition with potential for kidney damage. She was treated for the condition with, inter alia, Prednisolone, a corticosteroid drug. At a point when the plaintiff was under the defendant’s care another drug, Dexamethasone, was substituted for Prednisolone. However, the defendant did not prescribe a “steroid sparer”, Imuran being suggested. The trial judge found that by changing the drug and not prescribing Imuran the defendant breached his duty of care to the plaintiff.

It was agreed at the trial that the ingestion of corticosteroid drugs had caused the plaintiff to suffer from vertebral microfractures following the development of osteoporosis in the plaintiff’s spine. However, the trial judge held that the plaintiff had failed to prove damages resulting either from the failure to introduce Imuran or from the prescription of Dexamethasone.

The conclusions of the trial judge are included in the judgment of Campbell AJA in the Court of Appeal. The trial judge said that he “was not persuaded on the balance of probabilities that had Imuran been introduced … the fractures … would have been prevented.” His Honour concluded: “I am not persuaded on the balance of probabilities that the plaintiff did lose the chance of a better outcome because of the failure to introduce Imuran at the relevant time.”

Campbell AJA records that it was apparently accepted at trial and on appeal that should the facts support a case that the appellant lost the chance of a better outcome “it was available in point of law.” The trial judge formulated the question in these terms: “In order to recover damages for the loss of a chance of a better outcome, the plaintiff is required to prove on the balance of probabilities that there did exist a chance that the plaintiff would have had a better outcome had the negligence in treatment not occurred: see Malec v J C Hutton Pty Ltd (1990) 169 CLR 638; Sellars v Adelaide Petroleum NL (1994) 179 CLR 333; Daniels v Anderson (1995) 37 NSWLR 438; and Tran v Lam (Badgery-Parker J, 20 June 1997, unreported). Has the plaintiff proved on the balance of probabilities that there did exist a chance that the introduction of Imuran on or about 10 June would have resulted in a better outcome, if not by avoiding the occurrence of the fractures then at least by reducing their severity? If so, then, ‘unless the chance is so low as to be regarded as speculative – say less than one percent’ ( Malec (at 643)), the plaintiff is entitled to recover an appropriate award of damages referable to the quantification of the loss of the chance.”

Approaching the factual determination with a “robust and pragmatic” approach to the primary facts of the case Campbell AJA determined that the excess of corticosteroid caused the loss of a chance that the appellant would have suffered less spinal damage than she in fact did. His Honour held that the chance lost was “more than speculative or remote” and, although it was a chance of substance, it “would fall short of a fifty one percent chance.”

Both the other members of the court delivered reasoned judgments. Hodgson JA agreed with the orders proposed by Campbell AJA. His Honour said that the trial judge had not erred “in not being satisfied, on the balance of probabilities, that the breaches of duty by the respondent, which he found to have occurred, caused the fractures suffered by the appellant.” However, Hodgson JA also found that there was evidence which strongly supported a conclusion that the negligence increased a pre-existing risk that fractures would occur, giving rise to the question whether the plaintiff was entitled to be compensated “for the loss of the chance that, but for the negligence, the fractures would not have occurred (or would not have occurred at the time or with the severity of their actual occurrence).” His Honour reviewed decisions in both Australia and England relevant to the question and ultimately determined that on the authority of Malec v J C Hutton Pty Ltd (1990) 169 CLR 638 and Sellars v Adelaide Petroleum NL (1992) 179 CLR 332 it is enough to establish liability in personal injury cases if a plaintiff proves on the balance of probabilities that by reason of the defendant’s breach of duty he or she has been deprived of a valuable chance.

Critical to his Honour’s reasoning is the following paragraph: “That chance must be inherent in the circumstances, not merely an artefact of the way evidence is presented in the case. Thus, if it appears to be a plain fact as to whether treatment would or would not have been successful, and the element of uncertainty arises merely from different expert views, then the plaintiff will not be compensated for the chance that one expert might be correct. On the other hand, if it appears that the very best medical science can do is to say that the treatment had a quantifiable chance of success, then in my opinion that can be treated as a valuable chance for the loss of which a plaintiff can be compensated. As with other questions concerning causation, a common sense approach should be taken to the question of whether a valuable chance has been lost, or whether the situation is rather one where one or other alternative would definitely have occurred, and the only uncertainty is due to imperfections in the evidence.”

I confess, with respect, to some difficulty with his Honour’s remarks. If by using the term “plain fact” his Honour meant that the evidence in a particular case allowed of a determination on the balance of probabilities that the treatment would or would not have been successful, this must occur in every case. However, it will be a question which can usually be answered only after considering the evidence of experts who quite probably will disagree. In most cases, and the present is a good illustration of the problem, medical scientists are able to quantify the chance of success, although individual scientists disagree about the level at which it should be quantified.

Hodgson JA was not swayed by Gaudron J’s cautionary note in Naxakis v Western General Hospital & Anor (1999) 197 CLR 269 where her Honour said that allowing for the loss of a chance in medical negligence may disadvantage plaintiffs (279-280). His Honour thought that the approach required by Malec meant that a plaintiff’s case must be reconciled with the substantial chance that the adverse result could have resulted in any event.

In his reasons for judgment Santow JA carried out a comprehensive review of the existing authorities. His Honour was considering the problem before the House of Lords decided, in Gregg v Scott [2005] 2 AC 176, that medical negligence did not allow for recovery on the basis of a percentage reduction in the prospects of a favourable outcome, but his Honour noted that the English Court of Appeal had arrived at this conclusion in earlier proceedings ( Gregg v Scott [2002] EWCA Civ 1471). However, accepting that Malec was an indication that Australia was taking a different path, his Honour identified the fact that there are sound policy reasons why the law should embrace damage for loss of the chance of a successful outcome that is less than 50 percent. If it did not doctors would be relieved of legal responsibility whenever a patient had less than a 50 percent chance of a favourable outcome. Relevant decisions of the High Court

As I have related both Hodgson JA and Santow JA relied upon Malec. In that case the plaintiff, a meatworker, sued his employer in negligence after he contracted brucellosis. The trial judge found that the employer had been negligent as a result of which the plaintiff contracted this disease but also concluded that it was equally probable that the plaintiff’s supervening neurotic condition was either precipitated by brucellosis or attributable to other unrelated circumstances. In the Full Court this finding was reversed and it was held that his neurotic condition at the time of the trial was caused by depression induced by acute brucellosis. However, the majority concluded that, by reason of the plaintiff’s personality it was “likely that the development of symptoms from his deteriorating back condition [which it was found had not been caused by the defendant’s negligence] would have produced a similar neurotic condition even if he had never contracted his brucellosis.”

There was a joint judgment of Deane, Gaudron and McHugh JJ in the High Court in the course of which their Honours said (at 642-643): “When liability has been established and a common law court has to assess damages, its approach to events that allegedly would have occurred, but cannot now occur, or that allegedly might occur, is different from its approach to events which allegedly have occurred. A common law court determines on the balance of probabilities whether an event has occurred. If the probability of the event having occurred is greater than it not having occurred, the occurrence of the event is treated as certain; if the probability of it having occurred is less than it not having occurred, it is treated as not having occurred. Hence, in respect of events which have or have not occurred, damages are assessed on an all or nothing approach. But in the case of an event which it is alleged would or would not have occurred, or might or might not yet occur, the approach of the court is different. The future may be predicted and the hypothetical may be conjectured. But questions as to the future or hypothetical effect of physical injury or degeneration are not commonly susceptible of scientific demonstration or proof. If the law is to take account of future or hypothetical events in assessing damages, it can only do so in terms of the degree of probability of those events occurring. The probability may be very high — 99.9 per cent — or very low — 0.1 per cent. But unless the chance is so low as to be regarded as speculative — say less than 1 per cent — or so high as to be practically certain — say over 99 per cent — the court will take that chance into account in assessing the damages. Where proof is necessarily unattainable, it would be unfair to treat as certain a prediction which has a 51 per cent probability of occurring, but to ignore altogether a prediction which has a 49 per cent probability of occurring. Thus, the court assesses the degree of probability that an event would have occurred, or might occur, and adjusts its award of damages to reflect the degree of probability. The adjustment may increase or decrease the amount of damages otherwise to be awarded. See Mallett v McMonagle [1970] AC 166 at 174; Davies v Taylor [1974] AC 207 at 212-219; McIntosh v Williams [1979] NSWLR 543 at 550-551. The approach is the same whether it is alleged that the event would have occurred before or might occur after the assessment of damages takes place.

Their Honours’ remarks are entirely confined to the assessment of damages. Brennan and Dawson JJ agreed with the majority but expressed reservations about assessing damages “on the footing of an evaluation expressed as a percentage.” Their Honours were of the view that “damages founded on hypothetical evaluations defy precise calculation.” I do not otherwise understand their Honours to reject the views of the majority. They adopted the statement of Lord Diplock in Mallett v McMonagle [1970] AC 166 at 176 to the effect that when assessing damages which depend upon a view as to “what will happen in the future or would have happened in the future if something had not happened in the past, the court must make an estimate as to what are the chances that a particular thing will or would have happened and reflect those chances, whether they are more or less than even, in the amount of damages which it awards.”

In Malec there was no question that the defendant’s negligence had, on the balance of probabilities, caused the damage that the plaintiff had suffered. The question was how a court should approach the task of assessing damages when it was shown that it was more likely than not that at some point the plaintiff would have inevitably suffered the same type of injury that he suffered as a result of the defendant’s negligence. It was held that the plaintiff’s damages were to be discounted by the percentage chance that his injuries would have occurred for reasons unrelated to the defendant’s negligence. He was not to be denied damages entirely by applying the civil standard of proof to the hypothetical chance that his injuries would have occurred at a certain point in time irrespective of the defendant’s negligence. There was no suggestion in Malec that the plaintiff’s injury was actually the loss of a chance of a better medical outcome. The only chance that the court dealt with was the hypothetical chance that at some point after the injury was suffered the plaintiff would have suffered a similar injury due to independent causes.

Sellars followed Malec but in quite a different context. It related to a claim under the Trade Practices Act 1974 (Cth) . In their joint judgment Mason CJ, Dawson, Toohey and Gaudron JJ emphasised that causation is resolved by assessing the probabilities but if the loss was a commercial opportunity it is valued having regard to the possibilities. The joint judgment recognised that the loss of a commercial opportunity may have value, even if it could not be said, when it was lost, that on the balance of probabilities it would return a profit. Many speculative investments fail, others succeed, but at any given time they will have a value in the relevant market. Their Honours said (at 355-356): “Notwithstanding the observations of this Court in Norwest , we consider that acceptance of the principle enunciated in Malec requires that damages for deprivation of a commercial opportunity, whether the deprivation occurred by reason of breach of contract, tort or contravention of s 52(1), should be ascertained by reference to the court's assessment of the prospects of success of that opportunity had it been pursued. The principle recognized in Malec was based on a consideration of the peculiar difficulties associated with the proof and evaluation of future possibilities and past hypothetical fact situations, as contrasted with proof of historical facts. Once that is accepted, there is no secure foundation for confining the principle to cases of any particular kind. On the other hand, the general standard of proof in civil actions will ordinarily govern the issue of causation and the issue whether the applicant has sustained loss or damage. Hence the applicant must prove on the balance of probabilities that he or she has sustained some loss or damage. However, in a case such as the present, the applicant shows some loss or damage was sustained by demonstrating that the contravening conduct caused the loss of a commercial opportunity which had some value (not being a negligible value), the value being ascertained by reference to the degree of probabilities or possibilities. It is no answer to that way of viewing an applicant's case to say that the commercial opportunity was valueless on the balance of probabilities because to say that is to value the commercial opportunity by reference to a standard of proof which is inapplicable. The conclusion which we have reached on this question finds support in other considerations. The approach results in fair compensation whereas the all or nothing outcome produced by the civil standard of proof would result in the vast majority of cases in over-compensation or under-compensation to an applicant who has been deprived of a commercial opportunity. Furthermore, it is an approach which conforms to the long-standing practice of taking into account contingencies in the assessment of damages.”

The judgment of Brennan J in Sellars raises the potential for difficulties in applying the loss of a chance approach to personal injury cases. His Honour confirms the approach adopted in Malec but is careful to identify that the ultimate analysis may depend upon the loss that the plaintiff claims or at least how that loss is expressed. With respect, I confess some apprehension about a principle which evaluates the money sum to compensate an injured plaintiff differently depending on how it is pleaded.

This apprehension is shared by Baroness Hale of Richmond who in Gregg v Scott noted (at 233-234) some of the difficulties that arise when loss of a chance of a better outcome is pleaded in the alternative to the entire physical injury: “Almost any claim for loss of an outcome could be reformulated as a claim for loss of a chance of that outcome. The implications of retaining them both as alternatives would be substantial. That is, the claimant still has the prospect of 100% recovery if he can show that it is more likely than not that the doctor's negligence caused the adverse outcome. But if he cannot show that, he also has the prospect of lesser recovery for loss of a chance. If (for the reasons given earlier) it would in practice always be tempting to conclude that the doctor's negligence had affected his chances to some extent, the claimant would almost always get something. It would be a "heads you lose everything, tails I win something" situation. But why should the defendant not also be able to redefine the gist of the action if it suits him better? The appellant in this case accepts that the proportionate recovery effect must cut both ways. If the claim is characterised as loss of a chance, those with a better than evens chance would still only get a proportion of the full value of their claim. But I do not think that he accepts that the same would apply in cases where the claim is characterised as loss of an outcome. In that case there is no basis for calculating the odds. If the two are alternatives available in every case, the defendant will almost always be liable for something. He will have lost the benefit of the 50% chance that causation cannot be proved. But if the two approaches cannot sensibly live together, the claimants who currently obtain full recovery on an adverse outcome basis might in future only achieve a proportionate recovery. This would surely be a case of two steps forward, three steps back for the great majority of straightforward personal injury cases. In either event, the expert evidence would have to be far more complex than it is at present. Negotiations and trials would be a great deal more difficult. Recovery would be much less predictable both for claimants and for defendants' liability insurers. There is no reason in principle why the change in approach should be limited to medical negligence. Whether or not the policy choice is between retaining the present definition of personal injury in outcome terms and redefining it in loss of opportunity terms, introducing the latter would cause far more problems in the general run of personal injury claims than the policy benefits are worth.”

In no case has any member of the High Court suggested that the decision in either Sellars or Malec displaces the civil standard of proof in relation to causation in negligence. In Sellars itself Mason CJ, Dawson, Toohey and Gaudron JJ expressly said that “the general standard of proof in civil actions will ordinarily govern the issue of causation,” and Brennan J in his separate judgment (at 368) said that: “A constant standard of proof applies to the finding that a loss has been suffered and to the finding that the loss was caused by the defendant’s conduct, whether those findings depend on evidence of historical facts or on evidence giving rise to competing hypotheses. In any event, the standard is proof on the balance of probabilities.” Loss of a chance – the concept of vicissitudes

The common law faces a difficulty in providing a uniform approach to questions of causation and damage in cases of negligence. Although when a commercial opportunity is said to have been lost, quantification by calculation of the percentage chance of making a profit, acquiring an asset, or avoiding a loss is a familiar task, such concepts are entirely foreign in personal injury matters. A commercial opportunity will have a market value but the value of the percentage chance of a successful medical outcome allegedly lost, although personal to the plaintiff and no doubt of immense value to him or her, does not have the same value to others. It is not a chance which can be expressed to exist in a conventional market, or indeed in any market.

The difficulties in utilising the concept of the loss of a chance in personal injury cases arises against a background of a settled approach to causation and damages. Responsibility for a plaintiff’s injury will lie upon a defendant if the plaintiff can prove “that the defendant’s conduct materially contributed to the plaintiff suffering that injury:” Chappel v Hart (1998) 195 CLR 232 at 244 per McHugh J. Although in theory the contribution of the defendant to the plaintiff’s injury may have been less than 50%, if the contribution is nevertheless material the plaintiff will recover against that defendant. Materiality must be proved on the balance of probabilities. The problems encountered with proof were considered by the Court of Appeal in State of New South Wales v Burton [2006] NSWCA 12; and see: Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262; Elbourne v Gibbs [2006] NSWCA 127 esp. at [74]-[75].

It is accepted that damages in a personal injury matter should be assessed having regard to the vicissitudes of life and the pre-existing characteristics of the plaintiff. For this purpose assessments are made of the probability of a plaintiff living to a certain age, the prospects of working to an identifiable age, the possibility of independent accidents occurring and so on. Positive vicissitudes, such as the possibility of promotion, may also be taken into account. In a real sense this requires the court to assess the chance of future events occurring.

The modern approach to vicissitudes is summarised by Dawson, Toohey, Deane and Gummow JJ in Wynn v NSW Insurance Ministerial Corporation (1995) 184 CLR 485 at 497-498: “It is necessary to say something as to contingencies or ‘vicissitudes.’ Calculation of future economic loss must take account of the various possibilities which might otherwise have affected earning capacity. The principle and the relevant considerations were identified by Barwick CJ in Arthur Robinson (Grafton) Pty Ltd v Carter [(1968) 122 CLR 649 at 659] as follows: ‘Ill health, unemployment, road or rail accidents, wars, changes in industrial emphasis, so that industries move their location, or are superseded by new and different techniques, the onset and effect of automation and the mere daily vicissitudes of life are not adequately reflected by merely – and blindly – taking some percentage reduction of a sum which ignores them.’ It is to be remembered that a discount for contingencies or ‘vicissitudes’ is to take account of matters which might otherwise adversely affect earning capacity and as Professor Luntz notes, death apart, ‘sickness, accident, unemployment and industrial disputes are the four major contingencies which expose employees to the risk of loss of income.’ Positive considerations which might have resulted in advancement and increased earnings are also to be taken into account for, as Windeyer J pointed out in Bresatz v Przibilla [(1962) 108 CLR 541 at 544], ‘[a]ll “contingencies” are not adverse: all “vicissitudes” are not harmful.’ Finally, contingencies are to be considered in terms of their likely impact on the earning capacity of the person who has been injured, not by reference to the workforce generally. Even so, the practice in New South Wales is to proceed on the basis that a 15 per cent discount is generally appropriate, subject to adjustment up or down to take account of the plaintiff’s particular circumstances” (some references omitted).

Citing Malec and Sellars , amongst other decisions, Dawson, Toohey, Deane and Gummow JJ go on to say (at 498) that in order for a vicissitude to be taken into account, all that needs to be established is “a real possibility” of its occurrence. The relevant standard of proof is not the balance of probabilities. However, a court must not take into account as a “vicissitude” a benefit (such as a pension) that would have accrued to a plaintiff independently of his or her right of action and regardless of whether or not that right is enforced: Graham v Baker (1961) 106 CLR 340 at 343 per Dixon CJ, Kitto and Taylor JJ. And while it is appropriate to assess the possibility that an injury would have occurred regardless of the negligence due to a pre-existing condition and to discount the damages by the percentage arrived at (see, eg, Malec ), this does not alter the principle that the defendant must take the plaintiff as he finds him. As Dixon CJ said in Watts v Rake (1960) 108 CLR 158 at 160: “If the injury proves more serious in its incidents and consequences because of the injured man’s condition, that does nothing but increase the damages the defendant must pay. To sever the remaining leg of a one-legged man or put out the eye of a one-eyed man is to do a far more serious injury than it would have been had the injured man possessed two legs or two eyes.” When is the cause of action complete?

In the context of assessing damages for economic loss, Dixon CJ, Kitto and Taylor JJ said in Graham v Barker at 346-347 that: “A plaintiff’s right of action is complete at the time when his injuries are sustained and if it were possible in the ordinary course of things to obtain an assessment of his damages immediately it would be necessary to make an assessment of the probable economic loss which would result from his injuries. But for at least two obvious reasons it has been found convenient to assess an injured plaintiff’s loss by reference to the actual loss of wages which occurs up to the time of the trial and which can be more or less precisely ascertained and then, having regard to the plaintiff’s proved condition at the time of the trial, to attempt some assessment of his future loss. We mention this matter because it has been suggested that since an injured plaintiff is entitled to recover damages for the impairment of his earning capacity, the fact that a totally incapacitated plaintiff has, during the period of his incapacity, received his ordinary wages is not a matter to be taken into consideration. To be more precise, however, an injured plaintiff recovers not merely because his earning capacity has been diminished but because the diminution of his earning capacity is or may be productive of financial loss.”

This passage highlights one of the difficulties associated with the loss of a chance approach in the personal injury context. If the lost chance results in an injury that sounds in damages, then the right of action is complete at the time the injury is sustained. This means that the plaintiff’s right of action accrues some time before the occurrence of the ultimate physical injury upon which the lost chance is contingent. Gaudron J identified this conceptual difficulty. In Naxakis at 278, her Honour said: “Moreover, there is no reason in principle why loss of a chance or commercial opportunity should not constitute damage for the purposes of the law of tort where no other loss is involved. However, different considerations apply where, as here, the risk eventuates and physical injury ensues” (emphasis added).

In medical negligence cases the lost chance is inseparable from the physical injury. Unless and until the physical injury occurs, it cannot be concluded that the chance has gone. Suppose that a patient has a 40% chance of survival but through his doctor’s negligence this chance is reduced to 20%. Suppose further that, against the odds, the patient survives. Could the patient still recover damages for the lost chance? The lost chance of a better outcome is dependent on the adverse outcome occurring.

A lost chance of a better medical outcome is readily distinguished from a lost financial opportunity. Chaplin v Hicks [1911] 2 KB 786 was the first case in which loss of a chance was recognised as a type of compensable damage. It involved a competition for young ladies who wished to be actresses. Over six thousand ladies sent in their photographs, and the best 300 were published in a newspaper. The 50 “most beautiful” were selected by public vote, and each of these ladies was to attend an appointment with the defendant. From these 50 ladies, the defendant would select 12 whom he would engage for three years at various levels of pay. The plaintiff was voted one of the “most beautiful” 50, but through the defendant’s breach of contract she could not attend her appointment. The 12 winners were chosen from those who had had an appointment. The Court of Appeal concluded that the plaintiff had suffered a compensable loss. Vaughan Williams LJ said (at 793): “The jury came to the conclusion that the taking away from the plaintiff of the opportunity of competition, as one of a body of fifty, when twelve prizes were to be distributed, deprived the plaintiff of something which had a monetary value. I think that they were right and that this appeal fails.”

What the plaintiff lost in that case truly was a chance . She lost the chance to impress the defendant at an appointment, which deprived her of the opportunity to be one of the winners of the competition. The damage was complete at the moment she was denied an appointment. It had crystallised. There is no difficulty in finding on the balance of probabilities that the defendant’s breach of contract caused her to lose that chance. The quantum of the lost chance has nothing at all to do with whether or not the defendant’s breach of contract was causative of the loss.

The following passage from Laferrière at [89], which refers to the work of Jean Penneau (La Responsabilité Médicale, Paris, Sirey, 1977) illustrates the problem: “In order to make his argument clearer, Penneau transfers the chance analysis temporarily to the classical example of a student who, due to an accident, is prevented from taking an important career-related exam. According to the classical loss of a chance analysis, the individual who caused the accident will be required to indemnify the student for the loss of a real and serious chance of passing the examination and embarking on a career. The situation is entirely different, in Penneau’s view, where, despite the accident, the student attends the examination and fails: ‘Here, the chance has been tried, and we know that it has been lost; loss made concrete by the final damage – the failure, death or infirmity – with which it is precisely and necessarily confused.’ To speak, nonetheless, of a loss of chance in this situation would be to speak of the same damage in different and now irrelevant terms, according to Penneau.”

Baroness Hale of Richmond noted the difference between the two types of damage in Gregg at 232: “One counter-argument is that, in this as in many other respects, there is a real difference between personal injury and financial loss. As Tony Weir puts it: ‘where the claimant is suing in respect of personal injury or property damage, he must persuade the judge that that injury or damage was probably due to the defendant’s tort, whereas in case of financial harm it is enough to show that the claimant had a chance of gain which the defendant has probably caused him to lose. There is nothing irrational in this, unless one supposes it is sensible to speak of “loss of a chance” without saying what the chance is of. Losing a chance of gain is a loss like the loss of the gain itself, alike in quality, just less in quantity: losing a chance of not losing a leg is not at all the same kind of thing as losing the leg.’ It is unfashionable these days to distinguish between financial loss and personal injury. Losing the money one has may not be so different from losing the leg one has. But many claims for financial loss do not relate to the money one has but to the money one expected to have – a prospective financial gain. There is not much difference between the money one expected to have and the money one expected to have a chance of having: it is all money. There is a difference between the leg one ought to have and the chance of keeping a leg which one ought to have. There is perhaps an even greater difference between the disease free state one ought to have and the chance of having a disease free state which one ought to have.” The impact of the Civil Liability Act 2002 (NSW)

The Civil Liability Act 2002 (NSW) makes specific provision for the assessment of future economic loss, including a mandatory discount rate. It provides: 13 Future economic loss – claimant’s prospects and adjustments (1) A court cannot make an award of damages for future economic loss unless the claimant first satisfies the court that the assumptions about future earning capacity or other events on which the award is to be based accord with the claimant’s most likely future circumstances but for the injury. (2) When a court determines the amount of any such award of damages for future economic loss it is required to adjust the amount of damages for future economic loss that would have been sustained on those assumptions by reference to the percentage possibility that the events might have occurred but for the injury. (3) If the court makes an award of damages for future economic loss, it is required to state the assumptions on which the award was based and the relevant percentage by which damages were adjusted. 14 Damages for future economic loss – discount rate (1) If an award of damages is to include any component, assessed as a lump sum, for future economic loss of any kind, the present value of that future economic loss is to be determined by adopting the prescribed discount rate. (2) The ‘prescribed discount rate’ is: (a) a discount rate of the percentage prescribed by the regulations, or (b) if no percentage is so prescribed – a discount rate of 5%. (3) Except as provided by this section, nothing in this section affects any other law relating to the discounting of sums awarded as damages.”

Section 13 gives rise to significant issues when the injury alleged is the loss of a chance of a better medical outcome. It would seem that unless the chance of a better outcome is greater than 50%, there can be no award for future economic loss. This is because the plaintiff’s damages are based on what their future earning capacity would have been but for their injury ( Penrith City Council v Parks [2004] NSWCA 201 at [51]; cf MacArthur Districts MotorCycle Sportsman Inc v Ardizzone [2004] NSWCA 145 per Hodgson JA). If the relevant injury is the loss of a chance of a better outcome that is less than 50%, then on any view the plaintiff’s “most likely future circumstances but for the injury” will be that he or she would have suffered the physical injury anyway. That is, even if the chance had never been lost, it is still more likely than not that at the time of the trial the plaintiff would be in the same position. In such a case, “a court cannot make an award of damages for future economic loss.” On the other hand, if the lost chance was greater than 50% but less than 100%, any award for future economic loss must be discounted by the percentage chance that the ultimate physical injury would have occurred anyway (s 13(2)).

The position is otherwise where the alleged damage is loss of a financial opportunity. This is because in such a case the cause of action is complete at the time that the chance is lost. That is, the damages are not contingent upon the occurrence of some event after the chance is lost. It does not matter whether the opportunity turns out to be good or bad: the loss may be valued when the negligent breach occurs. The problem of causation

In Vairy v Wyong Shire Council (2005) 223 CLR 422 at 461, Hayne J observed that “[t]he inquiry into the causes of an accident is wholly retrospective. It seeks to identify what happened and why.” Causation is a question of what was i.e. did the defendant’s conduct cause the injury. To the extent that this involves any hypothetical questions, the answers to those questions only go to proof of the historical fact on the balance of probabilities (see Bennett v Minister of Community Welfare (1992) 176 CLR 408 at 422-423 per Gaudron J). The hypothetical questions are not themselves the facts in issue, although in a theoretical sense causation will always involve hypothetical questions. As Hayne J pointed out in Chappel at 282: “The search for causal connection between damage and negligent act or omission requires consideration of the events that have happened and what would have happened if there had been no negligent act or omission. It is only by comparing these two sets of facts (one actual and one hypothetical) that the influence or effect of the negligent act or omission can be judged.”

Unlike Sellars , Chappel v Hart was a personal injury case. It involved a failure to warn a patient about a risk of surgery that ultimately eventuated. There were five separate judgments. No member of the High Court decided the case on the basis of a lost chance. It was accepted that the injury in respect of which the plaintiff sought damages was her entire physical injury rather than the loss of a chance of a better medical outcome.

Gaudron J did not express an opinion about the role of a theory of loss of a chance in personal injury cases. McHugh J dissented but noted that the case did not fall within the principles defined in Sellars.

Gummow J (at 258-263) gave detailed consideration to the issue of loss of a chance. His Honour noted that Dr Chappel sought to avoid liability by arguing that Mrs Hart had lost no real and valuable chance of the risk of injury being diminished or avoided due to the defendant’s negligent failure to warn. His Honour then stated (at 258): “In this way the submissions of Dr Chappel tended to divert attention from the central issue, namely whether there was adequate reason in logic or policy for refusing to regard the ‘but for’ test as the cause of the injuries sustained by Mrs Hart, by the allurement of further cogitation upon the subject of ‘loss of a chance.’ Once the criterion for assessment of the adequacy of causation has been determined as a matter of law, the question whether the plaintiff has suffered some damage and therefore has a complete cause of action in tort is normally established by evidence which satisfies the civil standard of proof [ Sellars at 351, 353]. If causation is not established in this way, then the plaintiff will fail and recover nothing [ Sellars at 368].”

Gummow J noted that the traditional standard of proof of causation in negligence (which his Honour appears to accept was not disturbed by Sellars ) has led to difficulties in proving causation in some types of case. His Honour acknowledged that there has been some suggestion in other jurisdictions that these difficulties can be avoided by applying the loss of a chance analysis to causation. However, his Honour was concerned to emphasise that in Australia the loss of a chance analysis only affects the standard of proof at the stage of the assessment of damages. Gummow J stated (at 260) that: “… this is not a case in which Mrs Hart seeks damages for the loss of an opportunity or chance to acquire or receive a benefit with a value to be ascertained by reference to the degree of probabilities or possibilities. As is explained in Sellars v Adelaide Petroleum NL , in Australia this generally is what is involved in the ‘loss of a chance’ cases.”

And at 263: “In the present case, it would have been for Dr Chappel to show that Mrs Hart’s damages were to be reduced to reflect the possibility, being more than a speculation, that independently of his negligence Mrs Hart would have sustained at some later date the injuries of which she complained. That was not the way in which the case for the appellant [Dr Chappel] was presented. Rather, the attempt was to show a lack of causation and to deny any liability. The submissions by Dr Chappel in a large measure attempt to turn speculative matters, which are relevant, if at all, upon the assessment of damages, to account by disrupting the principles governing causation. In this Court, as in the Court of Appeal, Dr Chappel seeks an order setting aside the verdict for Mrs Hart and its replacement by a judgment in his favour. In any event, by her notice of contention Mrs Hart submits that Dr Chappel would have failed in any attempt to obtain a Malec discount and I agree. The evidence of Professor Benjamin, which is set out earlier in these reasons, and the observations in the Supreme Court of Canada to which I have referred, indicate the serious difficulty that would have arisen in this case in passing from the speculative to the ascertainment of a degree of probability. That consideration serves also to emphasise the strength of Mrs Hart’s case on causation.”

Kirby J is the only member of the court who indicated a preference for the loss of a chance approach in the context of causation, although his Honour expressed no concluded view. At 274-275 Kirby J said: “A further way in which, in some circumstances, the difficulties of causation for a plaintiff are alleviated is by treating the plaintiff’s loss as a ‘loss of a chance.’ In cases in which this approach is permissible, it may allow evaluation of the plaintiff’s loss in terms of comparing the chances of suffering harm (given the breach which has occurred) against those that would have existed (if the breach is hypothesised away). In CES v Superclinics (Aust) Pty Ltd [(1995) 38 NSWLR 47 at 56-57] I indicated my attraction to this approach as a more rational and just way of calculating damages caused by established medical negligence. It is clearly laid down by the authority of this Court that, in some circumstances, a plaintiff may recover the value of a loss of a chance caused by a wrongdoer’s act or omission. The approach also has some judicial support in the context of medical negligence in England, Canada and the United States. A number of commentators favour this approach because of the failure of orthodox reasoning to do justice to some patients’ losses and because it invites a more empirical calculation of loss, with the use of statistics which might offer outcomes that are more accurate and fair to all concerned. On the other hand, the weight of judicial opinion in England and Canada and some academic writing appears to be critical of the application of the loss of a chance theory to cases of medical negligence. In part this is because, where medical negligence is alleged, ‘destiny…[has] taken its course,’ arguably making an analysis by reference to chance inappropriate or unnecessary in the view of the critics of this approach. Alternatively, the loss of a chance calculation has been criticised on the ground that it would discard commonsense, undermine the plaintiff’s onus of proving the case and submit the law to the ‘paralysis’ of statistical abstractions.”

In marked contrast, Hayne J (at 289) took the view that the loss of a chance analysis should be rejected outright: “…how does one assess the value of the chance that has been lost? It was suggested in the course of argument that it is reflected in the assessment of damages by discounting the damages otherwise allowed. But that invites attention to what are those damages that are to be discounted – is it, as the argument appeared to assume, the damages attributable to the physical consequences which the respondent suffered? That could be so only if the physical consequences which the respondent suffered were caused by the appellant’s negligence. All of these considerations point to the conclusion that the loss of chance analysis is flawed and should not be adopted.”

Naxakis concerned a young lad who suffered a burst aneurysm in circumstances where it was alleged that if appropriate medical care had been provided the adverse outcome would have been avoided.

Although not necessary for her decision, Gaudron J considered whether the plaintiff could recover for the lost chance of a successful outcome. In doing so her Honour addressed some of the issues surrounding loss of a chance in the personal injury context . Her Honour accepted that in cases involving the failure to diagnose a pre-existing condition “there is no philosophical or logical difficulty in viewing the loss sustained as the loss of a chance” and accepted that this analysis may be “strictly correct.” However, in rejecting the approach that damages should be awarded on that basis her Honour, inter alia, observed that the lost chance approach cannot easily be applied in conjunction with the traditional balance of probabilities approach. Her Honour said at 280: “As already indicated, the lost chance approach requires proof that a valuable chance has been lost. A chance would have no value if the defendant could establish, on the balance of probabilities, that the pre-existing condition would have resulted in the injury or disability in question in any event. Thus, if proof on the balance of probabilities were also retained, damages for loss of a chance would be awarded only in those cases where the plaintiff cannot establish, on the balance of probabilities, that the risk would not have eventuated and the defendant cannot establish that it would. There is, thus, limited practical significance for an approach which allows for loss of a chance if the traditional approach is also retained.”

Gaudron J joined in the majority in Sellars, but in Naxakis her Honour was careful to limit the application of the loss of a chance analysis to cases involving loss of a commercial opportunity. In rejecting loss of a chance in personal injury cases her Honour observed that although it is usually justified in this context on the basis that it is a legitimate type of damage, the reality is that it is used to alleviate problems with uncertainty of causation: Naxakis at 278-279. The problem is expressed by the commentator Jacques Bore quoted by Gonthier J in Laferrière at [64]: “If therefore the compensation awarded is only partial, it is not because the death damage was itself partial: a dead person is not partly alive, and the victim or his heirs suffered the damage in its entirety; it is because the compensation is determined in relation to the probable causal link found to exist between the fault and the final damage. It is partial causation, determined in accordance with a probability calculation taking into account the influence of possible external factors, which gives rise to partial liability in this case…” (emphasis in original).

Gaudron J expressed the view in Naxakis that the difficulties of proving causation in medical negligence cases had been exaggerated (see 278-279) and that the concept of a lost chance was not required to overcome them. Her Honour confirmed (at 279) that where the defendant negligently creates or increases a risk of harm and that risk eventuates, the tribunal of fact is entitled to conclude that causation has been established on the balance of probabilities unless the defendant can establish that their breach had no effect or that the damage the plaintiff suffered was inevitable.

Callinan J was the only other member of the court in Naxakis who considered the issue of loss of a chance. His Honour also accepted McHugh J’s “material contribution test” and continued (at 312-313): “On the evidence here the jury were entitled to hold that the failure, the treating doctor’s omission to either undertake an angiogram or the failure to give any consideration to the undertaking of it, materially contributed to the appellant’s condition. They would be entitled to take an alternative view that the second respondent’s conduct, although it might not be possible to say (on the balance of probabilities) that it definitely materially contributed to the plaintiff’s final condition, at least caused him to lose a valuable chance (the value of which it was for them to assess) of avoiding being in the condition that he now finds himself. There is still, in my opinion, room for the operation of the loss of a chance rule (particularly in cases involving the practice of what is even today said to be an art rather than a scientific skill), enabling a plaintiff to recover damages to be equated with, and reduced to the value of the chance he or she has lost, rather than the damages which would be appropriate if it has been proved on the balance of probabilities that the plaintiff’s condition owes itself to the defendant’s acts or omissions.”

Callinan J’s analysis would seem to be consistent with subsequent authority in the NSW Court of Appeal.

When the conduct of a defendant is shown to have “materially contributed” to the plaintiff’s injuries causation on the balance of probabilities will be satisfied. The defendant, as a matter of legal proof, has caused the plaintiff’s entire injury. Where, however, all that can be shown is that the defendant’s breach of duty made some contribution to the plaintiff’s injury as opposed to a material contribution, then the only way that the plaintiff can succeed is on the basis of a lost chance of a better outcome. In State of New South Wales v Burton [2006] NSWCA 12 at [14], Spigelman CJ stated that: “I have set out [the trial judge’s] summary of the pertinent evidence of Dr Wright. That summary indicates that Dr Wright gave no evidence of any character on the basis of which the Court could assess the degree of contribution or the degree of increased risk. There was evidence from Dr Wright that the Appellant’s [i.e. the defendant’s] omissions made some contribution to the development of the PTSD itself. However, there was, in my opinion, no evidence which could justify an inference that that contribution was a material contribution. Furthermore, when one reads the reference to an increased ‘risk’ of developing PTSD in Dr Wright’s reports in their full context there is nothing to suggest that that increased degree of risk was significant” (emphasis in original).

His Honour concluded (at [24]) that “… the end result is that damages were assessed on an inappropriate basis. The matter should be remitted to the District Court for damages to be assessed on a loss of a chance basis” (see also the judgment of Basten JA at [66]). While his Honour agreed with Spigelman CJ’s opinion that the evidence in the case was insufficient to justify a finding of material contribution, Hunt AJA qualified his agreement by stating (at [91]) that: “…The Chief Justice has found…that the distinction drawn by Dr Wright between cause and contribution/exacerbation should be interpreted as reducing the extent of the contribution made to the respondent’s condition of post-traumatic stress disorder by the appellant’s omissions to something necessarily less than a material contribution…The word ‘exacerbation’ is generally used by the medical profession as meaning only that the original condition is made worse (or more serious), usually involving a greater intensity in the symptoms of that condition. That increase in severity may be minor, medium or extreme. The word exacerbation does not mean to me that the act which led to the exacerbation was necessarily something less than a material contribution to the condition exacerbated.”

Spigelman CJ had earlier considered the question of the proof necessary to satisfy the “material contribution” test in Seltsam . In that case, His Honour (at 280) accepted as fundamental the proposition that proof of “a mere possibility is not sufficient to establish causation for legal purposes.” However, evidence of a possibility is circumstantial evidence which, cumulatively, may amount to proof on the balance of probabilities or even beyond reasonable doubt. At [287] the Chief Justice approved the following passage from the judgment of Herron CJ in EMI (Australia) Ltd v BES [1970] 2 NSWLR 238 at 242: “Medical science may say in individual cases that there is no possible connexion between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be the touchstone, then the judge cannot act as if there were a connexion. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical evidence denies that there is any such connexion that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.”

The Chief Justice set out the passage from McHugh J’s judgment in Chappel v Hart that has been quoted above. His Honour said (at 279): “Although his Honour’s was a dissenting judgment, this passage has subsequently been referred to with approval: see Naxakis… per Gaudron J and…per Callinan J. The starting point of McHugh J’s analysis was that it had been established on the balance of probabilities that the conduct did create or increase the risk of injury, ‘and that risk had eventuated.’ This starting point is the very matter in issue in the present case. Was there evidence on the basis of which the trial judge could conclude, on the balance of probabilities, that there was an increased risk of injury and that that risk had ‘eventuated’ in the specific disease of the respondent? If there was such evidence then, to use the words of both Gaudron J…and Callinan J…the tribunal of fact was ‘entitled’ to find that the conduct which increased the risk, materially contributed to the injury – entitled, but not, of course, required to so find” (emphasis in original).

Importantly, his Honour stated (at 280) that: “There is a tension between the suggestion that any increased risk is sufficient to constitute a ‘material contribution,’ and the clear line of authority that a mere possibility is not sufficient to establish causation for legal purposes. The latter is too well-established to qualify the former. The reconciliation between the two kinds of references is to be found in the fact that, as in Chappel v Hart and in the cases that suggest the former, the actual risk had materialised. The ‘possibility’ or ‘risk’ that X might cause Y had in fact eventuated, not in the sense that X happened and Y also happened, but that it was undisputed that Y had happened because of X” (emphasis in original).

The effect is that evidence of a possibility that the relevant conduct caused the plaintiff’s injury is circumstantial evidence that may contribute to proof, on the balance of probabilities, of a material contribution. On the other hand, if the evidence taken as a whole does not establish anything more than a mere possibility that the conduct caused the injury, then causation has not been proved to the requisite standard of proof. Nevertheless, the plaintiff may still be entitled to receive damages on the basis of a lost chance. Does Rufo bind me in this case?

It is necessary to return to Rufo.

The Court of Appeal’s decision is, of course, binding on me. However, it was concerned with a chance that was assessed to be less than 50%. Santow JA (at 688-690) suggests that the loss of a chance analysis should also apply where the chance is greater than 50%. If this is the correct approach to causation it would displace the presently accepted standard of proof in medical negligence cases. The other judgments in the case are confined to defining a principle where the chance is less than 50%. Hodgson JA expressed (at 681) the view that the loss of a chance analysis should only apply to chances of less than 50%, while in cases where the plaintiff can prove causation on the balance of probabilities (i.e. where the chance is greater than 50%) Malec should continue to apply so that damages are assessed taking into account the percentage chance that the injury would have occurred in any event. Accordingly, insofar as “loss of a chance” presently has a place in personal injury cases on the current state of the law in New South Wales it is in cases where the plaintiff cannot prove causation on the balance of probabilities, and accordingly the lost chance is less than 50%. This is consistent with the view expressed by Callinan J in Naxakis, and with the approach adopted by Spigelman CJ in Burton. Conclusion in this case

I have already determined that on the balance of probabilities an ECG administered after 4 February would have revealed Kurt’s long QT. In my view the chances of that occurring were at least 65% and may have been greater. If his condition had been identified the chance that he would not have been effectively managed and a cardiac arrest avoided was negligible. Accordingly, the various plaintiffs have each made out their case and are entitled to verdicts in the sums agreed. Orders

Although damages have been agreed it may be necessary to consider matters of interest and costs. I direct the parties to bring in short minutes of order on which occasion any necessary submissions can be made.